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We quantified the lower extremity dynamics developed during the volleyball spike and block jumps to find out if predictive relations exist between jump dynamics and patellar tendinitis. Lower extremity movement biomechanics were analyzed for 10 members of the 1994 Canadian Men's National Volleyball Team (all right-handed hitters). Based on physical examination, 3 of the 10 players had patellar tendon pain associated with patellar tendinitis at the time of testing. In masked biomechanical and logistic regression analyses, we discovered that the vertical ground-reaction force during the take-off phase of both spike and block jumps was a significant predictor of patellar tendinitis-correctly predicting the presence or absence of patellar tendinitis in 8 of 10 players. Deepest knee flexion angle (during landing from the spike jump) predicted 10 of 10 cases correctly for the left knee. The external tibial torsional moment (during the takeoff for the right knee with the spike jump and for the left knee with the block jump) was also a significant predictor of tendinitis. In these players, the likelihood of patellar tendon pain was significantly related to high forces and rates of loading in the knee extensor mechanism, combined with large external tibial torsional moments and deep knee flexion angles.

In cells that exhibit apical growth, mechanisms that regulate cell polarity are crucial for determination of cellular shape and for the adaptation of growth to intrinsic and extrinsic cues. Broadly conserved pathways control cell polarity in eukaryotes, but less is known about polarly growing prokaryotes. An evolutionarily ancient form of apical growth is found in the filamentous bacteria Streptomyces, and is directed by a polarisome-like complex involving the essential protein DivIVA. We report here that this bacterial polarization machinery is regulated by a eukaryotic-type Ser/Thr protein kinase, AfsK, which localizes to hyphal tips and phosphorylates DivIVA. During normal growth, AfsK regulates hyphal branching by modulating branch-site selection and some aspect of the underlying polarisome-splitting mechanism that controls branching of Streptomyces hyphae. Further, AfsK is activated by signals generated by the arrest of cell wall synthesis and directly communicates this to the polarisome by hyperphosphorylating DivIVA. Induction of high levels of DivIVA phosphorylation by using a constitutively active mutant AfsK causes disassembly of apical polarisomes, followed by establishment of multiple hyphal branches elsewhere in the cell, revealing a profound impact of this kinase on growth polarity. The function of AfsK is reminiscent of the phoshorylation of polarity proteins and polarisome components by Ser/Thr protein kinases in eukaryotes.hyphal growth | protein phosphorylation | peptidoglycan | cytoskeleton | tip extension

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