Search

The fundamental aspect of tissue injury was the structural changes and functional disorders caused by a great deal of cell death, it might further develop into organ damage in severe cases. At present, the treatment of tissue injury was more focused on improving the micro-environment and promoting cell renewing. Insufficient attention was paid to the repair of cell damage, this oversight could exacerbate disease conditions and create difficulties in achieving healing. Thus, treating tissue injury should be based on repairing cell damage. In order to systematically grasp the research status and drug development of cell damage and repair, this article provided a systematic review of the damaging causes, repair mechanisms, and drug development from the perspectives of DNA damage, RNA damage, protein damage, mitochondrial damage, membrane damage and cell death. It was expected to contribute to promoting the research and development of repair medicines.

Placental diseases may affect the outcome of pregnancy and long-term health of the mother and fetus. Fetal fraction is a key indicator for the success of non-invasive prenatal testing, and has been associated with gestational age, body mass index and fetal chromosomal aneuploidies. Many studies have found that fetal fraction is also related to placenta-derived diseases and may become a new predictor for such diseases. This article has summarized the association between the two, with an aim to provide new ideas for the prediction of placental diseases.

The suitable experimental animal model is important in research of pathogenesis and therapeutic strategies of diabetic foot ulcer, and the murine model is the most commonly used one at present. It can be divided into two types: the animal model simulating pathological conditions and the model simulating clinical symptoms. This article reviews the current research progress on the mechanisms of diabetic ulcer pathogenesis, and relevant treatment strategies, including the inhibition of matrix metalloproteinases (MMPs) expression, promotion of angiogenesis and anti-inflammatory therapy.

Objective: To evaluate the value of a panel fluorescence in situ hybridization (FISH) in the detection of common chromosome abnormalities in myelodysplastic syndrome (MDS)., Methods: Twenty cases of MDS patients, whose karyotypes were unknown by the FISH examiner beforehand, were analyzed with a panel FISH using YAC248F5 (5q31), YAC938G5 (7q32), CEP8 and YAC 912C3 (20q12) probes to detect the frequently occurring chromosome abnormalities (-5/5q, -/7q-, +8, 20q-) in MDS. Then the results were compared to those of conventional cytogenetics (CC)., Results: Among 20 cases, 13 cases were found to carry common chromosome abnormalities by panel FISH (trisomy 8, five cases; -5/5q-, one case; 20q-, five cases; 5q- accompanying 20q-, one case; complex abnormalities, one case). However, on CC examination, only five cases were found to have common chromosomal abnormalities (20q-, four cases; 5q- accompanying 20q-, one case). In addition, trisomy 21, marker chromosome and complex abnormalities comprising -5, -7 and marker chromosomes were seen in one case each, the rest were normal., Conclusion: Panel FISH is a useful tool of molecular cytogenetics in the detection of common chromosome abnormalities in MDS.

Objective: To study the origin of aberrant clones with chromosome abnormalities in MDS., Methods: Antibodies recognizing myeloid cells (CD33), B cells (CD19) and T cells (CD2) were used to sort bone marrow cells of ten MDS patients with chromosome abnormalities (trisomy 8 five cases, trisomy 8 accompanying trisomy 9 one case, trisomy 8 accompanying 7p- one case, 20q- two cases, t (1; 7) one case) by Immuno-Magnetic Bead technique, then the positive cells for CD33, CD19 or CD2 were detected respectively by interphase FISH using the centromeric probes for chromosomes 1, 7and 8, and the locus specific probe for 20q12. 200 to 300 cells were scored for each detection., Results: FISH showed that trisomy 8, t (1; 7) and 20q- all affected CD33 positive cells, but not CD2 positive cells in these ten MDS patients. Only in one MDS patient, 20q- affected the CD19 positive cells., Conclusion: Our data suggest that the chromosomal aberrations in MDS are mostly restricted to myeloid cell lineages, but B lymphocytes are involved in minor MDS implying that abnormal clone originated from a multipotent hematopoietic progenitor.

Objective: To study the myelodysplastic syndrome(MDS) with 1;7 translocation in five cases and to determine further the constitution and origin of centromere of the derivative chromosome resulting from 1;7 translocation., Methods: Bone marrow chromosome preparation of five cases was made using direct method or short- term culture. Karyotypic analysis was carried out by R-banding technique. Dual-color fluorescence in situ hybridization(FISH) using Spectrum Red and Spectrum Green directly labeled chromosome 1-specific a-satellite DNA probe(red) and chromosome 7-specific a-satellite DNA probe(green) was performed in three patients of them., Results: All of the five cases had 1;7 translocation. The centromere of the derivative chromosome 7p/1q was constituted with red and green signals in three of them., Conclusion: The result of dual-color FISH confirms that the centromere of the derivative chromosome resulting from 1;7 translocation originated from both centromeres of chromosome 1 and chromosome 7.