No description available.

Cls cDNA clones, which together contained the entire coding region of the protein, were isolated from two human-liver cDNA libraries. The initial Cls clones were identified using a synthetic oligonucleotide probe which corresponded to a region of low degeneracy near the C-terminus of the Cls catalytic chain. Fragments of the Cls cDNA were used to screen a cosmid library in an attempt to isolate the Cls gene, but this proved unsuccessful and no positive clones were isolated. The complete primary sequence of Cls revealed that the homology between the Cls and Clr catalytic chains also extends throughout their non-catalytic chains. Like Clr, Cls can be divided into six structurally independent domains of which the sixth represents the catalytic B chain. Domains I and III in the A chain of Cls are internally homologous, as are domains IV and V. The latter domains are homologous to the internally repeating 60-residue sequences found in Factor B, C2 and other proteins. Domain II of Cls is similar to the 40-residue repeat sequences found in epidermal growth factor precursor and many of the vitamin K-dependent proteins. The assignment of these domains to the different regions of Cls tertiary structure has still to be achieved, but studies in this area should be facilitated now that the complete primary sequence for the Cls zymogen is available.

No description available.

Thesis (Ph.D.)--Tufts University, 2001. / Adviser: Juliet A. Fuhrman. Submitted to the Dept. of Biology. Includes bibliographical references. Access restricted to members of the Tufts University community. Also available via the World Wide Web;

Diss. (sammanfattning) Uppsala : Univ., 2003. / Härtill 5 uppsatser.

Thesis (M. Med. Sc.)--University of Hong Kong, 2010. / Includes bibliographical references (p. 55-61).

Thesis (Ph.D.) - University of Queensland, 2003. / Includes bibliography.

No description available.

Natural killer cell cytotoxic activity (NKCA) and the proportion of circulating natural killer (NK) cells were compared in 10 weight trainers versus 10 sedentary controls. Height, weight, and percent body fat did not differ significantly between the two groups. The average subject in the weight training group was able to squat 1.8 times his body weight, lifted weight more than 6 hours a week, and had been a weight trainer for nearly 9 years. NKCA did not differ between the weight training and control groups (166 ± 33 vs. 155 ± 27 lytic units, respectively), and the proportion of NK cells was the same (15.1 ± 1.9% vs. 15.1 ± 1.3%, respectively). The results of this cross-sectional study of long-term weight trainers and sedentary controls indicate no significant differences in NKCA. The two groups did not differ in the distribution of lymphocytes or natural killer cells, lending strength to this conclusion.

This study examined the acute and chronic effects of changes in training volume and intensity on the blood lymphocyte percentages and immunoglobulin levels in runners. Twelve runners participated in four 10-day phases over a 40 day training period. Phase 1 and phase 3 were "baseline" phases of low volume/low intensity running (LV/LI). Phase 2 and phase 4 consisted of either high volume/low intensity (HV/LI) or high volume/high intensity (HV/HI) training. Subjects were randomly assigned to one of 2 different crossover training group orders: 1) LV/LI, HV/LI, LV/LI, HV/HI or 2) LV/LI, HV/HI, LV/LI, HV/LI. HV/LI training involved doubling the LV distance run at the same LI of 60-70% V02 max. The HV/HI phase consisted of the same volume as the HV/LI phase, but alternate days were replaced with a series of high intensity 1000 m intervals (95-100% V02 max). Venous blood samples were drawn at rest on days 1, 4 and 7 and 5 minutes post-exercise on days 1 and 7 of each 10-day phase. Lymphocyte subsets were determined by flow cytometry using monoclonal antibodies for total T (CD3+), T-helper (CD4+), T-suppressor (CDS+) lymphocytes and HLA-DR+ (a B cell and "activated" T-lymphoid cell marker). IgA, IgG and IgM levels were obtained by ELISA analysis. This study revealed remarkable stability of humoral (antibody) immune components during and after runs of various intensities and volumes. Immunoglobulin levels were not significantly affected by alterations in volume or intensity over the 4 training phases. A transient decrease was observed in the T-lymphocyte percentages of CD3+, CD4+ and the CD4/CD8 ratio 5 minutes post-exercise which was significant (p <.05) during the HV/LI and HV/HI phases. Adaptation of lymphocyte subpopulations occurred with repeated exposure to increases in volume and intensity. A training order effect was suggested whereby an initial HI phase, was more immunosuppressive and possibly negated the effects of subsequent HV phases. Results indicate that the exercise-induced lymphocyte subset reduction is transient and suggest that the extent of the reduction is more dependent upon training intensity than volume, and the order of exposure to the high-intensity stimulus may determine the magnitude of subsequent responses. / Thesis / Master of Science (MSc)