Repair of injured articular and growth plate cartilage using mesenchymal stem cells and chondrogenic gene therapy.

Injuries to the articular cartilage and growth plate are significant clinical problems due to their limited ability to regenerate themselves. Despite progress in orthopedic surgery and some success in development of chondrocyte transplantation treatment and in early tissue-engineering work, cartilage regeneration using a biological approach still remains a great challenge. In the last 15 years, researchers have made significant advances and tremendous progress in exploring the potentials of mesenchymal stem cells (MSCs) in cartilage repair.

Intramembranous ossification mechanism for bone bridge formation at the growth plate cartilage injury site.

Salter's type III and type IV growth plate injuries often induce bone bridge formation at the injury site. To understand the cellular mechanisms, this study characterized proximal tibial transphyseal injury in rats. Histologically, bony bridge trabeculae appeared on day 7, increased on day 10, and became well-constructed on day 14 with marrow.

Roles of growth factors in chemotherapy-induced intestinal mucosal damage repair.

Chemotherapy agents induce apoptotic cell death and loss of cell proliferation in the intestinal crypt epithelium, resulting in intestinal mucosal damage called "mucositis". Small intestinal mucositis is characterized structurally by crypt loss and villus atrophy, and functionally by absorptive and barrier impairments. The increased use of chemotherapy in cancer treatment and the clinical importance of the intestinal mucositis as a common side effect have stimulated more active research into understanding the pathophysiology of intestinal mucositis and developing agents for preventing or treating this condition.

The molecular basis of X-linked spondyloepiphyseal dysplasia tarda.

The X-linked form of spondyloepiphyseal dysplasia tarda (SEDL), a radiologically distinct skeletal dysplasia affecting the vertebrae and epiphyses, is caused by mutations in the SEDL gene. To characterize the molecular basis for SEDL, we have identified the spectrum of SEDL mutations in 30 of 36 unrelated cases of X-linked SEDL ascertained from different ethnic populations. Twenty-one different disease-associated mutations now have been identified throughout the SEDL gene.

The role of complement, antibody, and tumor necrosis factor alpha in the killing of Plasmodium falciparum by the monocytic cell line THP-1.

Killing of Plasmodium falciparum blood forms by the differentiated human myelomonocytic THP-1Mo cell line was studied by a radiometric assay. Results showed that parasite killing was promoted by complement, antimalarial antibody, and the cytokines tumor necrosis factor alpha and gamma interferon. Differentiated THP-1Mo appears to be a useful monocytic cell line for the study of mechanisms of immunity to Plasmodium.

Effect of 22-32 carbon n-3 polyunsaturated fatty acids on superoxide production in human neutrophils: synergism of docosahexaenoic acid with f-met-leu-phe and phorbol ester.

Docosahexaenoic (22:6 n-3) and eicosapentaenoic acid (20:5 n-3) stimulated the oxygen-dependent respiratory burst in intact neutrophils in a dose-dependent manner as measured by either superoxide dismutase (SOD)-inhibitable cytochrome c reduction and lucigenin-dependent chemiluminescence. A number of longer chain hexaenoic acids isolated from ram testis (22 to 32 carbon fatty acids) showed a diminishing response with increasing carbon chain length. 22:6 acted synergistically to enhance the responses to two other neutrophil agonists, f-met-leu-phe (FMLP) and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).