OBJECTIVE: To explore the relationship between the expression change of cytokines and the wound age during the healing process of rats skin wound. METHODS: Immunohistochemical and image-analysis methods were performed on vital skin wounds(after incision 0.5-168 h am) and postmortem damage(after incision 0.5-6 h pm). RESULTS: The expression of the cytokines PDGF-beta, PDGFR-beta, TGF-beta 1, and bFGF in the epithelial cells was already enhanced since 0.5 h am after damage and their strongest expression reaction was seen at 24-96 h am. In addition, the expression of PDGF-beta, PDGFR-beta, TGF-beta 1 and bFGF was also found in the macrophages and the fibroblasts of the granulation tissue, and the expression changes in the postmortem damage group showed that the skin tissue within 0.5-3 h after incision showed immunohistochemical changes but weakly expression and 3 h thereafter no any change was found. CONCLUSION The expression characteristics of the above mentioned cytokines in wound repair should be related to the wound age and it reminds therefore that they may be used as immunohistochemical criteria for accurate determining the wound age.
Animals ; Cytokines/biosynthesis* ; Female ; Fibroblast Growth Factor 2/biosynthesis* ; Male ; Platelet-Derived Growth Factor/biosynthesis* ; Rats ; Rats, Wistar ; Receptor, Platelet-Derived Growth Factor beta/biosynthesis* ; Skin/metabolism* ; Time Factors ; Transforming Growth Factor beta/biosynthesis* ; Transforming Growth Factor beta1 ; Wound Healing

OBJECTIVETo identify clinical and laboratory abnormalities and genetic defect of Fechtner syndrome in a Chinese family.

METHODSThe characteristic morphological features of platelets and leukocytes were examined on blood smears with Wright's-Giemsa staining and ultrastructure of platelet and leukocyte were investigated under electron microscope. Genomic DNA was isolated from peripheral blood of the proband and 9 members of his family. All the exons and exon-intron boundaries of the MYH9 gene were amplified by PCR followed by direct sequencing.

RESULTSPatients presented the characteristic clinical features including macrothrombocytopenia, leukocyte inclusions and/or hereditary nephritis. A heterozygous C to T mutation was found in the proband and three members of his family at nucleotide 5981 in exon 40 of MYH9 gene, resulting in a nonsense mutation which encoded truncated protein due to premature termination at the Arg 1933 codon.

CONCLUSIONIt is the first report of a Chinese family with Fechtner syndrome. The Arg (CGA) 1933--> stop (TGA) nonsense mutation in MYH9 gene is a causative genetic defect.

Adult ; Codon, Nonsense ; DNA Mutational Analysis ; Exons ; genetics ; Humans ; Inclusion Bodies ; genetics ; Male ; Molecular Motor Proteins ; genetics ; Myosin Heavy Chains ; genetics ; Nephritis, Hereditary ; genetics ; Pedigree ; Syndrome ; Thrombocytopenia ; genetics