386 research outputs found

    Estimation of Fish Biomass Using Environmental DNA

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    Environmental DNA (eDNA) from aquatic vertebrates has recently been used to estimate the presence of a species. We hypothesized that fish release DNA into the water at a rate commensurate with their biomass. Thus, the concentration of eDNA of a target species may be used to estimate the species biomass. We developed an eDNA method to estimate the biomass of common carp (Cyprinus carpio L.) using laboratory and field experiments. In the aquarium, the concentration of eDNA changed initially, but reached an equilibrium after 6 days. Temperature had no effect on eDNA concentrations in aquaria. The concentration of eDNA was positively correlated with carp biomass in both aquaria and experimental ponds. We used this method to estimate the biomass and distribution of carp in a natural freshwater lagoon. We demonstrated that the distribution of carp eDNA concentration was explained by water temperature. Our results suggest that biomass data estimated from eDNA concentration reflects the potential distribution of common carp in the natural environment. Measuring eDNA concentration offers a non-invasive, simple, and rapid method for estimating biomass. This method could inform management plans for the conservation of ecosystems

    Lineage-specific RUNX3 hypomethylation marks the preneoplastic immune component of gastric cancer

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    Runt domain transcription factor 3 (RUNX3) is widely regarded as a tumour-suppressor gene inactivated by DNA hypermethylation of its canonical CpG (cytidine-phosphate-guanidine) island (CGI) promoter in gastric cancer (GC). Absence of RUNX3 expression from normal gastric epithelial cells (GECs), the progenitors to GC, coupled with frequent RUNX3 overexpression in GC progression, challenge this longstanding paradigm. However, epigenetic models to better describe RUNX3 deregulation in GC have not emerged. Here, we identify lineage-specific DNA methylation at an alternate, non-CGI promoter (P1) as a new mechanism of RUNX3 epigenetic control. In normal GECs, P1 was hypermethylated and repressed, whereas in immune lineages P1 was hypomethylated and widely expressed. In human GC development, we detected aberrant P1 hypomethylation signatures associated with the early inflammatory, preneoplastic and tumour stages. Aberrant P1 hypomethylation was fully recapitulated in mouse models of gastric inflammation and tumorigenesis. Cell sorting showed that P1 hypomethylation reflects altered cell-type composition of the gastric epithelium/tumour microenvironment caused by immune cell recruitment, not methylation loss. Finally, via long-term culture of gastric tumour epithelium, we revealed that de novo methylation of the RUNX3 canonical CGI promoter is a bystander effect of oncogenic immortalization and not likely causal in GC pathogenesis as previously argued. We propose a new model of RUNX3 epigenetic control in cancer, based on immune-specific, non-CGI promoter hypomethylation. This novel epigenetic signature may have utility in early detection of GC and possibly other epithelial cancers with premalignant immune involvement

    Detection and Characterization of Oncogene Mutations in Preneoplastic and Early Neoplastic Lesions

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    While it has been nearly 30 years since its discovery, the ras family of genes has not yet lost its impact on basic and clinical oncology. These genes remain central to the field of molecular oncology as tools for investigating carcinogenesis and oncogenic signaling, as powerful biomarkers for the identification of those who have or are at high risk of developing cancer, and as oncogene targets for the design and development of new chemotherapeutic drugs. Mutational activation of the K-RAS proto-oncogene is an early event in the development and progression of the colorectal, pancreatic, and lung cancers that are the major causes of cancer death in the world. The presence of point mutational "hot spots" at sites necessary for the activation of this proto-oncogene has led to the development of a number of highly sensitive PCR-based methods that are feasible for the early detection of K-RAS oncogene mutations in the clinical setting. In light of these facts, mutation at the K-RAS oncogene has the potential to serve as a useful biomarker in the early diagnosis and risk assessment of cancers with oncogenic ras signaling. This chapter describes a highly sensitive method for detecting mutant K-RAS, enriched PCR, and its application to early detection of alterations in this oncogene in preneoplastic and early neoplastic lesions of the colon and rectum

    Ultrasound biomicroscopy findings of 25 G Transconjuctival sutureless (TSV) and conventional (20G) pars plana sclerotomy in the same patient

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    BACKGROUND: Transconjunctival Sutureless Vitrectomy (TSV) is a recent advancement in vitreo-retinal surgical techniques involving the use of 25 G instruments through self-sealing sclerotomies. It has been hypothesized that there may be less chance of vitreous and retinal herniation in the scleral wound as compared to conventional sclerotomy incision. However there are no reports on differences in 20 gauge and 25 gauge sclerotomies using ultrasound biomicroscopy (UBM). We report herein the differences in sclerotomies undertaken with 20 gauge (G) and 25 gauge instruments in the same patient. CASE PRESENTATION: Ultrasound biomicroscopy of the sclerotomy sites was done in the same patient in whom both 20 G and 25 G sclerotomies had to be constructed during pars plana vitrectomy and the differences were studied. On day 2, we observed a wide gape at the site that had been enlarged using a 20G MVR blade. In contrast, the other two sites made transconjunctivally using the 25G trocar showed only a mild gape. Significant gape continued to persist at the subsequent evaluations on day 7 and day 14 only at the port, which had been enlarged. CONCLUSION: Healing of a 25 G sclerotomy is expectedly quite rapid, with inability to detect the site of sclerotomy in a short duration of 2 weeks post-operatively. This is as opposed to conventional sclerotomies, which might take up to 6–8 weeks post-operatively for complete opposition
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