Diabetic retinopathy (DR) is one of the leading causes of vision loss and can be effectively avoided by screening, early diagnosis and treatment. In order to increase the universality and efficiency of DR screening, many efforts have been invested in developing intelligent screening, and there have been great advances. In this paper, we survey DR screening from four perspectives: 1) public color fundus image datasets of DR; 2) DR classification and related lesion-extraction approaches; 3) existing computer-aided systems for DR screening; and 4) existing issues, challenges, and research trends. Our goal is to provide insights for future research directions on DR intelligent screening.

BACKGROUNDRecurrence or metastasis of myxomas is not rare and can lead to malignancy. We aimed to analyze the risk factors for postoperative cardiac myxoma recurrence and to summarize its clinical characteristics, treatments and classification.

METHODSThe clinical data of 5 patients with recurrent cardiac myxoma were retrospectively analyzed and our clinical experience was summarized. Moreover, the relevant literatures were reviewed.

RESULTSAll the five cases of primary myxomas were derived from atypical positions. One patient had early distant metastasis, one had family history, and two suffered malignant recurrence. The recurrence interval was (2.30 ± 2.16) years and the recurrent tumors were all found in different chambers from those of the corresponding primary tumors. Re-operation was performed after recurrence. One patient died of heart failure after malignant recurrence, and the other 4 cases had satisfactory therapeutic outcomes after re-operations. Our experience advocated a clinical classification of "typical" and "atypical" cardiac myxoma, the typical myxomas referred to the tumors locating at the left atria, with single pedicle, rooted at or around the fossa ovalis, involving no genetic causes, and the atypical myxomas included the familial tumors, tumors stemming from multiple chambers, rooted in abnormal positions of the left atrium, with evident genetic mutation, or with malignant tendency.

CONCLUSIONSPostoperative follow-up is of vital importance for patients with myxomas characterized by multi-chamber distribution, early distant metastasis, atypical origin, and family history. Once recurs, re-operation is necessary and should be performed immediately.

Adult ; Aged ; Female ; Heart Neoplasms ; diagnosis ; surgery ; Humans ; Male ; Middle Aged ; Myxoma ; diagnosis ; surgery ; Retrospective Studies ; Risk Factors

This study was purposed to investigate the effect of AML1-ETO fusion protein resulted from hematopoietic transcription factor (AML1) and acute myeloid leukemia M(2b)(AML-M(2b)) on transcription activity of nucleobindin 2 (nucb2) promoter, and to explore the role of AML1-ETO in molecular pathogenesis of AML-M(2b). The real-time RT-PCR was used to study the regulation of AML1-ETO on nucb2 at transcription level in AML1-ETO inducible leukemia cell line, the chromatin immunoprecipitation (ChIP)-based qPCR was used to investigate the direct in vivo interaction between the AML1, AML1-ETO and nucb2 promoter in AML1-ETO positive leukemia cell line, the luciferase report gene assay was used to detect the regulation of AML1, AML1-ETO on the transcription activity of nucb2 promoter. The results showed that the expression level of nucb2 was reduced with the increase of AML1-ETO. The promoter of nucb2 could be bound by both AML1 and AML1-ETO. The promoter of nucb2 was trans-repressed by AML1 and AML1-ETO respectively. It is concluded that the nucb2 is the direct target gene of AML1 and AML1-ETO, the transcription regulation of AML1, AML1-ETO on nucb2 is carried out via repressing its promoter activity.
Calcium-Binding Proteins ; genetics ; Cell Line, Tumor ; Core Binding Factor Alpha 2 Subunit ; genetics ; DNA-Binding Proteins ; genetics ; Gene Expression Regulation, Leukemic ; Humans ; Nerve Tissue Proteins ; Oncogene Proteins, Fusion ; genetics ; Promoter Regions, Genetic ; RUNX1 Translocation Partner 1 Protein ; Transcription Factors ; genetics ; Transcriptional Activation