Prolotherapy is an alternative injection-based therapy for chronic musculoskeletal pain. Three different proliferants, D-glucose (dextrose), phenol-glucose-glycerine (P2G), and sodium morrhuate, used in prolotherapy are hypothesized to strengthen and reorganize chronically injured soft tissue and decrease pain through modulation of the inflammatory process. Our hypothesis is that commonly used prolotherapy solutions will induce inflammation (leukocyte and macrophage infiltration) in medial collateral ligaments (MCLs) compared to needlestick, saline injection, and no-injection controls. MCLs of 84 Sprague-Dawley rats were injected one time at both the tibial and femoral insertions. Immunohistochemistry (IHC) was used to determine the inflammatory response at three locations (tibial and femoral insertions and midsubstance) 6, 24, and 72 h after dextrose injection compared to saline-and no-injection controls and collagenase (positive control) (n ¼ 4). qPCR was used to analyze gene expression 24 h postinjection (n ¼ 4). Sodium morrhuate, P2G, and needlestick control were also investigated after 24 h (n ¼ 4). In general, inflammation (CD43þ, ED1þ, and ED2þ cells) increased after prolotherapy injection compared to no-injection control but did not increase consistently compared to saline and needlestick control injections. This response varied by both location and proliferant. Inflammation was observed at 6 and 24 h postinjection but was resolved by 72 h compared to no-injection controls (p < 0.05). CD43þ leukocytes and ED2þ macrophages increased compared to needlestick and saline-injection control, respectively, 24 h postinjection (p < 0.05). Prolotherapy injections created an inflammatory response, but this response was variable and overall, not uniformly different from that caused by saline injections or needlestick procedures. ß

Background-Prolotherapy is an alternative therapy for chronic musculoskeletal injury including joint laxity. The commonly used injectant, D-glucose (dextrose), is hypothesized to improve ligament mechanics and decrease pain through an inflammatory mechanism. No study has investigated the mechanical effects of prolotherapy on stretch-injured ligaments.

The onset latency and discharge amplitude of preprogrammed postural responses were evaluated in order to determine if the structure of synergistic activation could be altered by ligamentous laxity at the knee joint. Twelve subjects with unilateral and one subject with bilateral anterior cruciate ligament (ACL) insufficiency were tested while standing on a moveable platform. External balance perturbations (6 cm anterior or posterior horizontal displacements of the platform) were presented at velocities ranging from 15 to 35 cm/s. Perturbations were presented under the following experimental conditions: unilateral and bilateral stance, knees fully straight or flexed, and with ankle motion restricted or free. These stance, knee position, and ankle motion conditions were introduced to alter the stress transmitted to the knee joint during movement of the support surface. The automatic postural response was recorded from the tibialis anterior (T), quadriceps (Q), and medial hamstrings muscles (H) bilaterally. The normal response to an externally induced backward sway involved the automatic activation of T and Q at latencies of 80 ms and 90 ms respectively. Activation of the hamstrings in the non-injured extremity was not coupled with the postural response. Hamstrings are not typically involved in the correction posterior sway because H activation would tend to pull the center of mass further backwards. However, when the response in the ACL-deficient extremity was compared to the non-injured limb: (1) the automatic postural response in the ACL-deficient extremity was restructured to include hamstrings activation (100 ms latency), (2) H activation time was faster and less variable in the ACL-deficient limb, and (3) the ratio of H/Q discharge amplitude integrated over 100 ms and 200 ms from the onset of EMG activation showed a dominance of hamstring activity during unilateral stance on the lax limb. In addition, H/Q ratios integrated over 200 ms showed dominant hamstring activity in the ACL-deficient limb during bilateral stance. (4) Cross-limb comparisons showed greater normalized IEMG amplitudes for T, H, and Q during unilateral stance on the lax limb. These results suggest that a capsular-hamstring reflex is integrated into the existing structure of a preprogrammed postural synergy in order to compensate for ligamentous laxity. Furthermore, the generalized increase of response gain observed during perturbations of unilateral stance on the lax limb indicates that joint afference can modulate central programming to control localized joint hypermobility. A concept of postural control is discussed with respect to the capsular reflex, joint loading and displacement of the center of gravity.

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Camera image sensors can be used to detect ionizing radiation in addition to optical photons. In particular, cosmic-ray muons are detected as long, straight tracks passing through multiple pixels. The distribution of track lengths can be related to the thickness of the active (depleted) region of the camera image sensor through the known angular distribution of muons at sea level. We use a sample of cosmic-ray muon tracks recorded by the Distributed Electronic Cosmic-ray Observatory to measure the thickness of the depletion region of the camera image sensor in a commercial smart phone, the HTC Wildfire S. The track length distribution prefers a cosmic-ray muon angular distribution over an isotropic distribution. Allowing either distribution, we measure the depletion thickness to be between 13.9 µm and 27.7 µm. The same method can be applied to additional models of image sensor. Once measured, the thickness can be used to convert track length to incident polar angle on a per-event basis. Combined with a determination of the incident azimuthal angle directly from the track orientation in the sensor plane, this enables direction reconstruction of individual cosmic-ray events.