Association between biological maturation and anterior cruciate ligament injury risk factors during cutting.

BACKGROUND: Adolescent females are particularly susceptible to suffering anterior cruciate ligament (ACL) injuries, likely influenced by well-established maturational changes. This study investigated ACL biomechanical injury risk factors and their association with biological maturation in females. METHODS: Thirty-five adolescent females (15±1 year) completed a series of maximum-effort 90° unanticipated cutting maneuvers. Established biomechanical ACL injury risk factors (including external knee abduction moments, knee abduction, hip abduction, knee flexion, ground reaction force) were derived from an optoelectronic motion analysis system and force platforms, with inter-limb asymmetries in these risk factors also computed. Biological maturation (percentage of predicted adult stature) was assessed using validated regression equations, incorporating anthropometric measures of participants and their biological parents. RESULTS: Significant bilateral asymmetries were observed with higher peak external knee abduction moments, higher ground reaction forces and less knee flexion (from 0-18% and 30-39% of contact) during the non-dominant vs. dominant cuts (effect sizes =0.36, 0.63 and 0.50, respectively). Maturation did not appear to influence these asymmetries; however, less hip abduction was observed (e.g., 21-51% of contact for dominant cuts) in more biologically-mature females. CONCLUSIONS: These results highlight a potential maturation-related change in cutting technique that may explain the apparent heightened ACL injury risk in this population. As females mature, training targeted at neuromuscular control of hip abductor (e.g. gluteal) muscle groups could potentially mitigate ACL injury risk.

Ia-restricted interaction between normal lymphoid cells and SJL lymphoma (RCS) leading to lymphokine production. I. Enhancement and suppression of antibody formation to TI antigens by supernatants and cells from cocultures of RCS and lymphoid cells.

Addition of gamma-irradiated reticulum cell sarcoma (RCS) cells causes suppression of the antibody response to trinitrophenyl (TNP)-keyhole limpet hemocyanin (KLH)-primed syngeneic SJL spleen cells to TNP-polyacrylamide (PAA) in vitro. The response of anti-brain antigen (BAT) + C-treated spleen cells is not suppressed by gamma-RCS, but is suppressed by cells from 48-hr SJL lymph node or thymus + gamma-RCS cultures. Addition of as few as 2.5 x 10(5) cultured (anti-I-A + C treated to remove gamma-RCS) cells causes significant inhibition of the responses of both syngeneic and allogeneic spleen cells. Treatment of gamma-RCS-induced suppressor cells with anti-BAT + C reduces their suppressive activity. In contrast to the cells, supernatants (SN) from (lymph node (LN) + gamma-RCS) cultures greatly enhance, in an antigen-dependent fashion, the responses of untreated or anti-BAT + C-treated Sephadex G10-passed spleen cells to TNP-PAA. TNP-SIII polysaccharide, or TNP-Ficoll, but not as much to TNP-KLH. Addition of SN as late as Day 3 of culture still causes about half as much enhancement as leaving SN in throughout the culture period, but it has no effect if left with the spleen cells for only the first day of culture. SN contains high levels of IL-2 and IFN-gamma; absorption with cells from an IL-2-dependent cytotoxic T-cell line removes the enhancing activity, while treatment with pH 2 to remove the IFN-gamma has no effect. SN from an IL-2-producing T-cell line (LBRM-33) has a similar effect on antibody production to TI antigens as does SN of (LN + gamma-RCS). The results suggest a marked dependency of PFC responses to TI antigen on IL-2 in all strains examined, including SJL, LAF1, DBA/2Ha, and CBA/N, probably through a direct activation of B cells. The findings also suggest that suppressor T cells, induced by gamma-RCS in syngeneic lymphoid cells, absorb the IL-2 needed for responses to TI antigens in vitro.

Role of B cells in the stimulation of syngeneic mixed lymphocyte responses.

Two different approaches were used to examine the role of B cells in the stimulation of syngeneic MLR. The relative inability of spleen and peritoneal exudate cells from B cell deficient mice, treated with anti-mu from birth, to serve as stimulator cells in SMLR was previously shown in SJL mice and confirmed in BALB/c mice in the present studies. Preincubation of cells from anti-mu treated mice with serum Ig does not enhance their ability to stimulate. Upon stimulation with normal spleen cells responses from anti-mu treated mouse T cells are not deficient. Responses of thymus cells from neonates and from adult cortisone-treated mice are also much higher when the splenic stimulator cells come from normal rather than from anti-mu treated mice. The deficiency of the stimulator cells from anti-mu treated mice is in the high density cell population as obtained after BSA gradient fractionation of collagenase treated lymph node or spleen fragments. Low density populations from anti-mu treated and normal mice stimulate equally well. Addition of exogenous IL-2 to the cultures enhances the syngeneic MLR to all stimulator populations and allows stimulation by spleen cells from anti-mu treated mice. It is concluded that, while B cells represent the major stimulator cell population in whole spleen cell suspensions, other accessory cells (dendritic cells?) are more efficient, possibly synergize with B cells by producing IL-1, but usually represent only a minor subpopulation. The other approach concerns the effectiveness of SMLR stimulation by several tissue culture, cloned B lymphoma cell lines, and by a transplantable BALB/c B lymphoma. Of the five stimulating lymphoma cell lines only one stimulates approximately as well in the absence as in the presence of polyethylene glycol. These latter cells (A20.1.11) can also stimulate T cell proliferation and IL-2 production in the absence of Ia+ accessory cells in the responding population and, therefore, either produce their own IL-1 or are able to bypass the requirement for this lymphokine.

Effect of histoincompatibility on migration of labeled bursa cells in the chicken.

A comparison was made of the localization of i.v. injected 3H-adenosine-labeled bursa cells in gamma-irradiated B-identical and B-different recipient chickens. There was no difference in the localization in nonlymphoid organs or in bursa and thymus, but the spleen showed more radioactivity at 24 hr after injection in B-identical than in B-different recipients. This difference was more reproducible in 3 to 4 week or older than in 7- to 10-day-old recipients. Histologically, the greatest difference in the older recipients was seen in the number of labeled cells localizing in germinal centers of spleen. Thymectomy or bursectomy of recipients did not appear to affect the bursa cell localization. syngeneity at the major histocompatibility B locus between donor and recipients appeared sufficient to obtain maximal spleen localization of donor bursa cells.

Growth of SJL/J-derived RCS as related to its ability to induce T cell proliferation in the host. II. Negative influence of H-2d1.

Backcross SJL x (SJL x BALB/c)F1 and (SJL x BSVS)F1 mice were examined for their ability to support growth of transplantable SJL lymphoma (reticulum cell sarcoma (RCS). A marked linkage to H-2 was noted in that H-2s/d backcross mice failed to support tumor growth, while H-2s/s backcross mice showed approximately 70% of the growth seen in SJL mice, as judged by lymph node and spleen weights. Spleen cells obtained from backcross mice by splenectomy were examined for their ability to give proliferative responses to gamma-RCS cells, whereafter individual splenectomized mice were also examined for their ability to support lymphoma growth. Both properties showed a similar degree of linkage to H-2 and to each other, although there seemed to be a segregating non-H-2 BALB gene which also exerted an additional, less marked negative influence on the proliferative responses. It is suggested that the proliferative response in vivo may contribute to the lymphoma growth and that the presence of H-2d is inhibitory. (SJL x BSVS)F1 mice gave excellent proliferative responses and supported growth of RCS to approximately 80% of those of controls. These results confirm previous conclusions on the negative effect of H-21d in F1 hybrids on both phenomena.