Performance in dynamic movement tasks and occurrence of low back pain in youth floorball and basketball players.

BACKGROUND: Prospective studies investigating risk factors for low back pain (LBP) in youth athletes are limited. The aim of this prospective study was to investigate the association between hip-pelvic kinematics and vertical ground reaction force (vGRF) during landing tasks and LBP in youth floorball and basketball players. METHODS: Three-hundred-and-eighty-three Finnish youth female and male floorball and basketball players (mean age 15.7 ± 1.8) participated and were followed up on for 3 years. At the beginning of every study year the players were tested with a single-leg vertical drop jump (SLVDJ) and a vertical drop jump (VDJ). Hip-pelvic kinematics, measured as femur-pelvic angle (FPA) during SLVDJ landing, and peak vGRF and side-to-side asymmetry of vGRF during VDJ landing were the investigated risk factors. Individual exposure time and LBP resulting in time-loss were recorded during the follow-up. Cox's proportional hazard models with mixed effects and time-varying risk factors were used for analysis. RESULTS: We found an increase in the risk for LBP in players with decreased FPA during SLVDJ landing. There was a small increase in risk for LBP with a one-degree decrease in right leg FPA during SLVDJ landing (HR 1.09, 95% CI 1.02 to 1.17, per one-degree decrease of FPA). Our results showed no significant relationship between risk for LBP and left leg FPA (HR 1.04, 95% CI 0.97 to 1.11, per one-degree decrease of FPA), vGRF (HR 1.83, 95% CI 0.95 to 3.51) or vGRF side-to-side difference (HR 1.22, 95% CI 0.65 to 2.27) during landing tasks. CONCLUSIONS: Our results suggest that there is an association between hip-pelvic kinematics and future LBP. However, we did not find an association between LBP and vGRF. In the future, the association between hip-pelvic kinematics and LBP occurrence should be investigated further with cohort and intervention studies to verify the results from this investigation. LEVEL OF EVIDENCE: Prognosis, level 1b.

Investigation of knee control as a lower extremity injury risk factor: A prospective study in youth football.

This prospective study in youth football examined the relationship between frontal plane knee projection angle (FPKPA) during the single-leg squat and sustaining an acute lower extremity injury or acute non-contact lower extremity injury. Secondly, side-to-side asymmetry in FPKPA and sex as injury risk factors were explored. In addition, we investigated the influence of age, sex, and leg dominance on the FPKPA. A total of 558 youth football players (U11 to U14) participated in the single-leg squat test and prospective injury registration. FPKPA was not found as a risk factor for injuries at this age. There was no difference in the mean FPKPA between sexes. However, FPKPA was associated with age; oldest subjects displayed the smallest FPKPA. Among boys, the frontal plane knee control improved by age. Among girls, the relationship between age and FPKPA was not as clear, but the oldest girls displayed the smallest mean FPKPA in the study (12.2° ± 8.3°). The FPKPA was greater on the dominant kicking leg compared to the non-dominant support leg (P < .001 for boys, P = .001 for girls). However, side-to-side asymmetry in FPKPA was not associated with future injuries. In conclusion, frontal plane knee control in the single-leg squat was not associated with lower extremity injuries among young football players. As the single-leg squat to 90° knee flexion was too demanding for many subjects, easier single-leg squat test procedure or a different movement control test, such as a double-legged squat, could be more suitable for the young football players.

Carbon nanotube network varactor.

Microelectromechanical system (MEMS) varactors based on a freestanding layer of single-walled carbon nanotube (SWCNT) films were designed, fabricated and tested. The freestanding SWCNT film was employed as a movable upper patch in the parallel plate capacitor of the MEMS. The measurements of the SWCNT varactors show very high tunability, nearly 100%, of the capacitance with a low actuation voltage of 10 V. The functionality of the varactor is improved by implementing a flexible nanocellulose aerogel filling.

Somatostatin analog lanreotide inhibits myocyte replication and several growth factors in allograft arteriosclerosis.

Chronic rejection is the most common reason for late loss of a transplant. The molecular mechanism of chronic rejection is not known and there is no treatment for this disorder. The characteristic histological feature in chronic rejection is increased smooth muscle cell replication in the vascular wall, leading to allograft arteriosclerosis. In this study we demonstrate that nonimmunosuppressed rat aortic allografts undergoing chronic rejection synthesize increased quantities of several smooth muscle cell growth-promoting substances in the vascular wall including interleukin-1, eicosanoids, and several peptide growth factors. Administration of a stable somatostatin analog lanreotide, BIM 23014, strongly inhibits myocyte proliferation in the allograft in vivo. It has no inhibitory effect on the proliferation of smooth muscle cells in vitro. Concomitantly, the locally produced peptide growth factors, i.e., epidermal growth factor, insulin-like growth factor 1, and BB-isomer of platelet-derived growth factor, but not other mediators of inflammation, are significantly reduced. The results suggest that growth factors are the main effector molecules leading to myocyte proliferation in allograft arteriosclerosis and that allograft arteriosclerosis (chronic rejection) may be specifically inhibited by lanreotide administration.

Chronic rejection in the rat aortic allograft. V. Mechanism of the angiopeptin (BIM23014C) effect on the generation of allograft arteriosclerosis.

Synthetic cyclic octapeptide analogues of somatostatin, such as angiopeptin (BIM23014C; AP) inhibit myointimal proliferation in chronically rejecting rabbit and rat allografts and following angioplasty in rabbits. We have investigated the mechanism of angiopeptin inhibition of allograft arteriosclerosis. DA (RT1a) aortic allografts were transplanted to WF (RT1v) recipients, which either received 80 micrograms/kg/day of AP (Alzet mini-pumps, s.c., 0-180 days) or were left untreated. AP administration did not affect the intensity of adventitial inflammation, nor reduced the disappearance of smooth-muscle cell nuclei from the media (media necrosis); however, it reduced their appearance in the intima and intimal thickening. The effect disappeared, however, from the 3rd month onward. In vivo labeling with tritiated thymidine and autoradiograms demonstrated that AP reduced slightly the proliferation of the inflammatory cells in adventitia and of smooth-muscle cells in the media, and reduced strongly and significantly (P < 0.01) the proliferation of smooth-muscle cells in the intima. Analysis of the major chronic-rejection associated eicosanoids from the vascular wall showed that AP had no effect on the release of the pro-inflammatory thromboxane B2 from the allograft. As AP did not reduce the intensity of perivascular inflammation, reduced only slightly the proliferation of inflammatory cells, and did not affect the release of thromboxane B2 from the inflammatory macrophages, it is likely that the AP effect is not directed to the inflammatory cells. As previous in vitro studies have demonstrated that vascular smooth-muscle cells proliferate in response to several growth factors, and as somatostatin analogues are inhibitory to their action, our data suggest that the action of AP on allograft arteriosclerosis is due to a direct effect on smooth-muscle-cell proliferation.

Effect of platelet-activating factor (PAF) receptor blockers on smooth muscle cell replication in vitro and allograft arteriosclerosis in vivo.

Platelet-activating factor (PAF) stimulates smooth muscle cell (SMC) replication both in vivo and in vitro. In this study we have investigated whether PAF receptor-blocking molecules modulate SMC replication in vitro and the generation of allograft arteriosclerosis in vivo. SMC cultures were established from baby rat aorta media and fibroblast control cultures from the adventitia. Identification of the cultured cell types was determined both by immunohistochemistry and electron microscopy. Both cell types replicated in culture with 10% fetal calf serum (FCS). The addition of PAF-C18 enhanced, and the addition of three PAF receptor inhibitors--WEB 2086, WEB 2170, and BN 50739--reduced, SMC replication and protein synthesis in a dose-dependent fashion in vitro until toxic concentrations were reached. The most potent of these drugs, WEB 2170, was then delivered at the rate of 12 mg/kg per day to recipients of rat aortic allografts. The responses were quantitated by autoradiography after short-term labeling of the recipients with tritium-labeled thymidine (3H-TdR) and by quantitative morphology. Administration of the PAF receptor blocker had no impact on the replication of the inflammatory cells in the allograft adventitia nor on the replication of SMCs in the media and intima. Administration of the PAF receptor blocker delayed the generation of allograft arteriosclerosis slightly, but not significantly. These results suggest that PAF is not an essential component in the inflammatory cascade leading to allograft arteriosclerosis.

Chronic rejection of rat aortic allografts. III. Synthesis of major eicosanoids by vascular wall components and effect of inhibition of the thromboxane cascade.

We have previously demonstrated that rat aortic allografts from the DA (RT1a) to the WF (RT1v) strain develop chronic arteriosclerotic changes in the vascular wall after a short spontaneously reversible acute rejection episode. These changes, which are lacking in syngeneic DA-to-DA control grafts, are virtually identical with those observed in human allografts during chronic rejection. In this study we have investigated whether eicosanoids are involved in the generation of arteriosclerotic changes. Incubation of aortic wall rings in vitro and immunochemical assays demonstrated that the arteriosclerotic allografts synthesize significantly more thromboxane B2 (TxB2) but not 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) or leukotriene B4. The increased synthesis of TxB2 in the allografts persisted for at least 5 months after transplantation. Separate incubation of the two major components of the vascular wall, after microdissection of the intima and (media plus) adventitia, demonstrated that most of the synthesis of TxB2 during chronic rejection was due to the outer layer of aorta, presumably the inflammatory cells of the adventitia. In contrast, most of the 6-keto-PGF1 alpha was synthesized by the inner layer of the aorta, presumably the endothelial cells and the smooth muscle cells of the intima. Administration of 1 mg.kg-1 x day-1 of a specific TxA2 receptor inhibitor, GR32191B, to the recipient rat reduced the proliferative response of inflammatory cells in the adventitia by 30%, as detected by in vivo tritiated-thymidine (3H-TdR) labeling and autoradiography, but did not reduce the proliferative response of smooth muscle cells in the media and intima.(ABSTRACT TRUNCATED AT 250 WORDS)

Towards understanding the pathophysiology of chronic rejection.

Chronic allograft rejection is the major reason why allografts are lost. While only 2%-3% of all allografts are lost during the first year to irreversible acute rejection, approximately 6%-7% are lost during each subsequent year to chronic rejection. The major manifestation of chronic rejection in all organs is persistent perivascular inflammation and allograft arteriosclerosis. Bearing this in mind, we have developed a model to investigate the pathophysiology of allograft arteriosclerosis using aortic transplantations between inbred rat strains. The results obtained thus far indicate that several different inflammatory cascades are operative within the vascular wall during allograft arteriosclerosis. The relative importance of these different cascades, and particularly the role of growth factors as final effectors, has not yet been defined. Attempts to suppress allograft arteriosclerosis under experimental conditions have already met with some success: under conditions where no immunosuppression is provided we have been able to delay the process by at least 3 months, though we have not been able to block it indefinitely. It may be expected, however, that once the inflammatory cascades leading to smooth muscle cell replication in the allograft media and their influx into the intima are better defined, more specific approaches to the inhibition of allograft arteriosclerosis will be developed.

Chronic rejection of rat aortic allografts: effect of inhibition of the thromboxane cascade.

Non-immunosuppressed rat aortic allografts from DA (RT1av1) to WF (RT1u) strain develop, after a short reversible acute rejection episode, chronic arteriosclerotic changes in the vascular wall, which are indistinguishable from those seen in human allografts during chronic rejection. Incubation of the aortic wall segments in vitro and immunochemical assays demonstrated that the allografts synthesized increased amounts of TxB2, but not 6-keto-PGF1alpha, or LTB4, compared to syngenic or normal aortas. The two major cellular components of the vascular wall, intima and adventitia, were incubated separately after microdissection. TxB2 was produced in the adventitia, whereas most of the 6-keto-PGF1alpha was synthesized in the intima. Administration of a specific TxA2 receptor inhibitor to the recipient rat reduced significantly the proliferation of adventitial inflammatory cells and the intimal smooth muscle cells. Nevertheless, it only delayed but did not inhibit the overall sclerosis of the intima.