Thesis (Ph. D.)--University of Missouri-Columbia, 2000. / Typescript. Vita. Includes bibliographical references (leaves 189-242). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 1999. / Typescript. Vita. Includes bibliographical references (leaves 92-107). Also available on the Internet.

Having considered the data collected thus far concerning immediate and delayed hypersensitivity reactions in the mouse, the experimentation following is devised essentially to follow the pattern of Crowle in the production and testing for immunoresponse. Instead of using the normal solvent, that is, acetone, this work is also intended to partially evaluated the use of dimethyl sulfoxide as a solvent for the contact allergin, dinitroflurobenzene.

Thesis (Ph.D.)--Boston University / Myostatin (mstn) belongs to the TGF-β family and is best known as a negative regulator of muscle growth. Hypermuscularity in mstn knockout mice has been widely recognized and numerous mstn inhibitors are in development to treat sarcopenia associated with aging and muscle wasting associated with chronic illness. To determine the health impact of long term mstn deficiency on physical performance, myostatin null (mstn-/-) mice were studied at three aging time points (5, 15, 22 months). Long term complete inhibition of myostatin was hypothesized to prevent the decline in physical performance expected with aging. The data disproves this hypothesis. While increased muscle was observed in the mstn-/- and the mice demonstrated an expected grip strength advantage at 5 months, by 15 and 22 months the overall grip strength was reduced with no significant difference compared to controls. Horizontal and vertical ambulatory activity at each aging time point showed a significantly decreased or a decreased trend when compared with age-matched wild type controls. Furthermore, the mstn-/- mice treadmill endurance was significantly less at 5 and 22 months and demonstrated a decreased trend at 15 months when compared to age-matched controls. Overall, long term myostatin deletion does not aid in the maintenance of overall physical performance as the animal ages. Since prior studies had also shown that myostatin affected both bone mass, cartilage development and skeletal tissue repair the effects of myostatin deletion were next examined relative to skeletal tissue structure and function. Micro Computerized Tomography (MicroCT) analysis showed increased size and ossification of the meniscus surrounding the knee, ectopic ossification surrounding the tarsal bones and extra ossification in joints between manus carpal bones in the myostatin null mice. These studies showed that this ectopic calcification increased with aging. Corresponding histology of 22 month old mstn-/- mice demonstrated increased fibrocartilage proliferation of the meniscus and loss of the tibial articular cartilage. Our current data suggests long term complete deletion of myostatin increases proliferation and differentiation of fibrocartilage and reduces articular cartilage maintenance leading to impaired joint function and an overall reduction in physical performance.

Includes list of publications produced during the period of candidature / Includes bibliographical references (leaves 254-274) / xiv, 274 leaves : ill. (col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Animal Science, 2003

Thesis (M. Med. Sc.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 42-45).

Thesis (M. Phil.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 67-80).

No description available.

The efficient processing of replication-dependent histone mRNA requires the Stem-Loop Binding Protein (SLBP). SLBP is also involved in regulating histone mRNA half-life, their nucleocytoplasmic transport, and their translation. Unlike somatic cells, where SLBP protein accumulates only in S-phase, SLBP protein is present throughout the first two embryonic cell cycles in mice. We report here that in late 2-cell mouse embryos there is a substantial, proteasome-dependent decrease in SLBP throughout the cell. Based on chromosome morphology, the degradation of SLBP protein in late 2-cell embryos is most likely a late G2-phase event. The degradation of SLBP protein is not simply a zygotic clock event, but requires development to the late 2-cell stage. Furthermore, SLBP protein degradation in 2-cell mouse embryos requires cyclin-dependent kinase (Cdk) activity, DNA replication, and zygotic genome activation. A model for SLBP protein degradation is proposed based on observations made in both early mouse embryos and somatic cells.

No description available.