BACKGROUND Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, resulting in the coronavirus disease COVID-19) is highly transmissible among people. Asymptomatic infections are also an important source of infection. Here, we aimed to further clarify the epidemiologic and clinical characteristics of asymptomatic SARS-CoV-2 infections. METHODS We identified close contacts of confirmed COVID-19 cases in northeast Chongqing who were RT-PCR+ yet remained asymptomatic throughout their infections. We stratified this cohort by normal versus abnormal findings on chest CT, and compared the strata regarding comorbidities, demographics, laboratory findings, viral transmission and other factors. RESULTS Between January and March, 2020, we identified and hospitalized 279 RT-PCR+ contacts of COVID-19 patients. Of these, 63 (23%) remained asymptomatic until discharge; 29 had abnormal and 34 had normal chest CT findings. The mean cohort age was 39.3 years, and 87.3% had no comorbidities. Mean time to diagnosis after close contact with a COVID-19 index patient was 16.0 days (range 1 to 29), and 13.4 days and 18.7 days for those with abnormal and normal CT findings, respectively (p < 0.05). Nine subjects (14.3%) transmitted the virus to others; 4 and 5 were in the abnormal and normal CT strata, respectively. The median length of nucleic acid turning negative in asymptomatic COVID-19 patients was 13 days, compared to 10.4 days in those with normal chest CT (p < 0.05). CONCLUSIONS A portion of these asymptomatic individuals, with and without abnormal chest CT scans, were capable of transmitting the virus to others. Given the frequency and potential infectiousness of asymptomatic infections, testing of traced contacts is essential. Studies of the impact of treatment on asymptomatic RT-PCR+ individuals on disease progression and transmission should be undertaken.
Ninety-four bone and soft tissue tumors were analyzed for their DNA content using flow cytometry (FCM). A simple, rapid method for preparing isolated nuclear suspensions was used. Tissues, minced in a hypotonic solution containing detergent and propidium iodide as a fluorescent probe for DNA, provided in most instances high nuclear yields from only 0.02 to 0.03 g of solid tumor. Whereas all nonneoplastic samples had a diploid DNA content, various degrees of abnormal DNA distributions were detected in 90% of the neoplastic samples and were present in benign as well as malignant tumors. Our findings demonstrate that FCM DNA analysis is practical in most musculoskeletal tumors and support the observations of others that abnormal DNA content may serve as a general neoplastic marker in these tumors.
In vitro cultures of a highly metastatic B16 melanoma clone (BL6-10) were found to undergo dramatic changes in morphology and differentiation upon transfer to another culture medium. Specifically, BL6-10 melanoma cells which had been originally selected and adapted for growth in Eagles' Hanks' amino acid supplemented media with 10 per cent newborn calf serum were amelanotic and epitheliod in shape. When these cells were shifted into Dulbecco's modified Eagles medium with 10 per cent fetal calf serum, they became highly melanotic and of spindle/dendritic morphology within 4 days of culture. These morphological changes as well as other parameters were all characteristic of established criteria of melanoma differentiation. Alterations in the differentiation state of our highly metastatic variant, BL6-10, did not result in any change in tumorigenicity but did have profound effects on metastatic potential. All of the morphological and functional characteristics of the differentiated melanoma were found to be reversible by re-plating the cells in their original growth medium and 4 days of in vitro growth. These studies have allowed us to follow and more firmly establish Met-72 antigen expression as a surface marker for metastatic cells of the B16 melanoma, and have provided direct experimental evidence that the less differentiated, Met-72 positive melanoma form is the dominant cell type capable of metastatic potential.
Two widely used B16 melanoma cell lines of low and high lung colonizing potential (B16-F1 and B16-F10) were compared in their ability to induce platelet aggregation. The results of these experiments showed a reproducible difference in platelet aggregating activity of these two cell lines which directly correlated with their lung colonizing potentials. However, when clones were derived from these heterogeneous cell lines and tested for experimental metastatic potential, platelet aggregating ability and Met-72 expression, no correlation could be attached to the platelet aggregating activity of the clones. Results of these experiments provide direct evidence that platelet aggregation is not an accurate index of experimental metastatic potential of tumor cell clones, nor is it an essential trait of all metastatic cells. The ability of tumor cells to induce platelet aggregation is examined and discussed in the context of cellular heterogeneity.
Aberrant DNA methylations have been reported to be significantly associated with lung squamous cell cancer (LUSC). The aim of this study was to investigate the DNA methylation-driven genes in LUSC by integrative bioinformatics analysis. In the present study, methylation-driven genes in LUSC were screened out, and survival analysis related to these genes was performed to confirm their value in prognostic assessment. Gene expression and methylation data were downloaded from The Cancer Genome Atlas (TCGA), and the MethylMix algorithm was used to identify methylation-driven genes. ConsensusPathDB was used to perform Gene Ontology and pathway enrichment analysis of methylation-driven genes. Survival analysis was performed to investigate the correlation with prognosis. In total, 52 differentially expressed methylation-driven genes were identified in LUSC and adjacent tissues. Survival analysis showed that DQX1, GPR75, STX12, and TRIM61 could serve as independent prognostic biomarkers. In addition, the combined methylation and gene expression survival analysis revealed that the combined expression level of the genes ALG1L, DQX1, and ZNF418 alone can be used as a prognostic marker or drug target. Methylation of four sites of gene ZNF418, four sites of ZNF701, two sites of DQX1, and four sites of DCAF4L2 was significantly associated with survival. The present study provides an important bioinformatic and relevant theoretical basis for subsequent early diagnosis and prognostic assessment of LUSC.
B16-F1 melanoma cells were plated onto plastic tissue-culture dishes rendered non-adhesive for cells by coating with 0.12 per cent poly(2-hydroxyethyl methylacrylate), poly(HEMA). These growth conditions caused the normally flat, adherent B16-F1 cells to grow as single cells in suspension. Within 24 hours, the rounded cells formed aggregates and grew at a slower rate than control cells grown at the same density on untreated plastic dishes. Microscopic observations provided evidence that polykaryocytosis was occurring among the aggregates. Following replating onto standard adhesive tissue-culture plastic, 20-30 per cent of the aggregates were observed to contain varying numbers of multinucleated giant cells (polykaryocytes). The study has revealed a previously undescribed propensity of certain B16-F1 cells cultivated as aggregates in suspension to develop into polykaryocytes, most probably as a result of spontaneous tumor cell-tumor cell fusion. The possible relevance of this behavior in vitro to events in tumor progression is discussed. This study, however, does not support the findings of others that the metastatic capability of B16-F1 cells is increased by such non-adherent culture conditions. No increase in metastatic potential was observed for B16-F1 cells, or for a low metastatic clone (F1-7) derived from it, grown for 72 or 96 hours in a spherical configuration compared to control cells grown in a flat, adherent monolayer.
Lung cancer is the most common type of cancer and the leading cause of cancer-associated death worldwide. Despite the availability of various treatments such as surgery, chemoradiotherapy, targeted drugs and immunotherapy, treatment is expensive and the prognosis remains poor. At present, lung cancer drugs and treatment programs remain in a state of continuous exploration and research to improve the prognosis, and to reduce the pain and economic burden for the patients. Type 2 diabetes is a common chronic disease in middle-aged and elderly patients, leading to significantly increased complications of cardiovascular and cerebrovascular diseases. Epidemiology shows that type 2 diabetes also increases the incidence of malignant tumors, including lung, liver, colorectal and pancreatic cancer. Metformin is a biguanide, widely used as a first-line oral drug in treating type 2 diabetes. Metformin has a hypoglycemic effect and a biological antitumor impact, reducing the incidence of various tumors, including lung cancer, and improving the prognosis of patients with tumors. The anti-lung cancer effect of metformin involves a variety of mechanisms that can improve the therapeutic effect and prognosis of lung cancer, as a single drug or in combination with other therapies. The present study aims to review the associated literature and the therapeutic effects of metformin on lung cancer. Contents 1. Introduction 2. Mechanisms of metformin in the treatment of lung cancer 3. Application of metformin in lung cancer treatment 4. Limitations and challenges of using metformin in lung cancer 5. Conclusion
Analysis of a number of B16 melanoma clones has revealed a high correlation between metastatic activity and the quantitative expression of a 72,000 dalton glycoprotein, Met 72. In the present study, metastatic tumor cell variants have been directly isolated from a heterogeneous, poorly metastatic melanoma (B16-F1) by anti-Met 72 monclonal antibodies and cell sorting procedures. These studies provide direct proof that Met-72 antigens are in fact surface markers of B16 melanoma metastatic variants and may provide the means of monitoring their presence, influence and autonomy during tumor progression.
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