Assessment of Humeral Retroversion Angle in Baseball Players: A Chronological Study

The objective of this study was to compare the humeral retroversion angles (HRA) between baseball players, including children, and those without a history of playing baseball, clarify the characteristics of the HRA in baseball players, and to determine whether or not chronological changes of the HRA are affected by a throwing motion. We studied 32 young baseball players (Group A), 10 elementary and junior high school students who had never played competitive overhead throwing sports (Group B), 65 adult baseball players who had been playing baseball since childhood in a little league or boy\u27s baseball team (Group C), and 11 adults who had never played competitive overhead throwing sports such as baseball or handball (Group D). Computed tomography of both humeri in these subjects was taken with a 5mm slice thickness. For the measurement of HRA, slices from the center of the humeral head and slices from the humeral epicondyle were examined. In baseball players, the mean HRA on the throwing side was larger than that on the non-throwing side, regardless of age and carrier. The HRAs of the elementary and junior high school baseball players as well as those of adult baseball players were larger on the throwing side. The HRA of the throwing side was significantly greater than that of the non-throwing side in both groups of baseball players. Furthermore, the mean HRA on the throwing side of young baseball players was significantly larger than that of adult baseball players, suggesting that the adaptive bony change of the humerus was caused by throwing stress and might occur in the early formative years of a player\u27s career

Determination of In-vivo Glenohumeral Translation during Loaded and Unloaded Arm Elevation

An understanding of normal joint kinematics is essential to develop treatments that restore normal joint mechanics; however, reports of kinematics during dynamic motion are rare. This study thus investigated glenohumeral (GH) translation in vivo during loaded and unloaded shoulder abduction. Nine healthy shoulders were studied from our patient cohort (average age, 31 years). We created 3D models of the scapula and humerus using computed tomography (CT) images and recorded fluoroscopic images during active abduction in neutral rotation in the plane of the scapula using a hand-held 3kg weight or no additional load. 3D motions were determined using model-based 3D-to-2D registration. Glenohumeral translation was determined by finding the location on the humeral head with the smallest separation from the plane of the glenoid. The humerus moved an average of 2 mm during arm abduction, from inferior to the center of the glenoid. There were no statistically significant differences between the unloaded and loaded conditions. Variability in humeral translation decreased with abduction using both 3-kg and 0-kg conditions, with significantly lower variability showing above a 70° GH abduction. We showed that humeral translation to the center of the glenoid maximizes joint congruency for optimal shoulder function and joint longevity. This data should lead to better strategies for shoulder injury prevention, enhanced rehabilitation, and improved surgical treatments

Hypothalamic GPR40 signaling activated by free long chain fatty acids suppresses CFA-induced inflammatory chronic pain.

GPR40 has been reported to be activated by long-chain fatty acids, such as docosahexaenoic acid (DHA). However, reports studying functional role of GPR40 in the brain are lacking. The present study focused on the relationship between pain regulation and GPR40, investigating the functional roles of hypothalamic GPR40 during chronic pain caused using a complete Freund's adjuvant (CFA)-induced inflammatory chronic pain mouse model. GPR40 protein expression in the hypothalamus was transiently increased at day 7, but not at days 1, 3 and 14, after CFA injection. GPR40 was co-localized with NeuN, a neuron marker, but not with glial fibrillary acidic protein (GFAP), an astrocyte marker. At day 1 after CFA injection, GFAP protein expression was markedly increased in the hypothalamus. These increases were significantly inhibited by the intracerebroventricular injection of flavopiridol (15 nmol), a cyclin-dependent kinase inhibitor, depending on the decreases in both the increment of GPR40 protein expression and the induction of mechanical allodynia and thermal hyperalgesia at day 7 after CFA injection. Furthermore, the level of DHA in the hypothalamus tissue was significantly increased in a flavopiridol reversible manner at day 1, but not at day 7, after CFA injection. The intracerebroventricular injection of DHA (50 µg) and GW9508 (1.0 µg), a GPR40-selective agonist, significantly reduced mechanical allodynia and thermal hyperalgesia at day 7, but not at day 1, after CFA injection. These effects were inhibited by intracerebroventricular pretreatment with GW1100 (10 µg), a GPR40 antagonist. The protein expression of GPR40 was colocalized with that of β-endorphin and proopiomelanocortin, and a single intracerebroventricular injection of GW9508 (1.0 µg) significantly increased the number of neurons double-stained for c-Fos and proopiomelanocortin in the arcuate nucleus of the hypothalamus. Our findings suggest that hypothalamic GPR40 activated by free long chain fatty acids might have an important role in this pain control system

FFAs profile in the hypothalamus tissue.

<p>FFAs were analyzed with UHPLC-MS/MS using MRM; FFA profile in the hypothalamus of intact mice (A). The FFA composition ratio of palmitate (C16:0), stearate (C18:0), oleinic acid (C18:1), linoleic acid (C18:2), arachidonic acid (C20:4) and DHA (C22:6) at day 1 with or without flavopiridol injection (B) and day 7 after CFA injection (C). Data, mean ± S.E.M., Saline n = 4, CFA (Day 1) (n = 7), CFA (Day 1)+flavopiridol (15 nmol) (n = 4), CFA (Day 7) (n = 4); ^#<i>p</i><0.05, compared with Saline (Scheffe's test), *<i>p</i><0.05, compared with CFA (Scheffe's test).</p

Antinociceptive effect of GW9508 and DHA on CFA-induced mechanical allodynia and thermal hyperalgesia.

<p>GW9508 (1.0 µg) and DHA (50 µg) i.c.v. administered in CFA-injected mice, whereas GW1100 (10 µg) was administered via the i.c.v. route 10 min before GW9508 or DHA injection; CFA-induced mechanical allodynia and thermal hyperalgesia are examined at day 1 (A, B) and 7 (C, D) post-injection; data, mean ± S.E.M.; Saline (n = 6), CFA (Day 1) (n = 6), CFA (Day 1)+GW9508 (1 µg) (n = 6), CFA (Day 1)+GW9508 (10 µg) (n = 6), CFA (Day 1)+GW9508 (25 µg) (n = 6), CFA (Day 1)+GW9508 (25 µg) (n = 6), CFA (Day7) (n = 6), CFA (Day 7)+GW9508 (1 µg) +GW1100 (1 µg) (n = 6), CFA (Day 7)+GW9508 (1 µg) +GW1100 (10 µg) (n = 6), CFA (Day 7)+DHA (50 µg) (n = 6), CFA (Day 7)+DHA (50 µg)+ GW1100 (10 µg) (n = 6); ^$<i>p</i><0.05, compared with saline; *<i>p</i><0.05, compared with CFA; ^#<i>p</i><0.05, compared with CFA+GW9508 (Scheffe's test).</p

Development of hyperplasia, mechanical allodynia and thermal hyperalgesia after CFA injection.

<p>CFA (10 µL, 0.5 mg/ml) was injected into the plantar surface of a mouse hind paw. Intraplantar injection of CFA elicited persistent hyperplasia (A), mechanical allodynia (B) and thermal hyperalgesia (C) for day 14; data, mean ± S.E.M., Saline (n = 12), CFA (n = 12); ^##<i>p</i><0.01, compared with saline (Student's <i>t</i>-test); ◊, saline; and ▪, CFA.</p

GW9508 injection activates POMC neuron, and releases β-endorphin in the arcuate neucrei of hypothalamus.

<p>Colocalization of GPR40 with POMC (a proopiomelanocortin neuron marker) and β-endorphin (A). Colocalization in the hypothalamus was evaluated with double immunofluorescence staining (green: GPR40; red: POMC; or red: GPR40, green β-endorphin). Scale bars: 10 µm. GW9508 administration causes induction of c-Fos protein in the arcuate nucleus. Confocal microscopic images of neurons double-labeled with POMC and c-Fos in the arcuate nucleus of the hypothalamus following the administration of GW9508 (1 µg/mouse, i.c.v.) (B). The image shows high magnifications of colocalization of neurons double-labeled with POMC and c-Fos in the arcuate nucleus of the hypothalamus (C) (green: c-Fos; red: POMC). Scale bars: 10 µm. Data summary is shown on the bottom, data, mean ± S.E.M.; Saline (n = 5), GW9508 (n = 5); *<i>p</i><0.05, compared with Saline (D). Immunofluorescence staining for β-endorphin in the hypothalamus following the administration of GW9508. Scale bars: 50 µm (E).</p

Effect of flavopiridol on CFA-elicited hyperplasia, GFAP increase, persistent mechanical allodynia and thermal hyperalgesia.

<p>Flavopiridol (5 and 15 nmol) was administered by i.c.v. injection into the left lateral ventricle of the mice twice a day (at 9:00 and 19:00) after CFA treatment. Hyperplasia of paw tissue was measured by means of a digital caliper (A). Representative Western blots of GFAP and GAPDH levels in the hypothalamus after CFA injection with or without flavopiridol are shown (B). Mechanical allodynia was evaluated using von Frey filaments (C). Thermal hyperalgesia of the hind paw was assessed using the plantar test (D); data, mean ± S.E.M.; Saline (n = 6), CFA (Day 7) (n = 6), CFA (Day 7)+flavopiridol 5 nmol (n = 6), CFA (Day 7)+flavopiridol 15 nmol (n = 6); ^#<i>p</i><0.05, ^##<i>p</i><0.01, ^###<i>p</i><0.001, compared with saline; * <i>p</i><0.05, *** <i>p</i><0.001, compared with CFA (Scheffe's test).</p

Effect of flavopiridol on CFA-elicited hyperplasia, GFAP increase, persistent mechanical allodynia and thermal hyperalgesia at day 7 after CFA injection.

<p>Flavopiridol (5 and 15 nmol) was administered by i.c.v. injection into the left lateral ventricle of the mice twice a day (at 9:00 and 19:00) after CFA treatment. Hyperplasia of paw tissue was measured by means of a digital caliper (A). Representative Western blots of GPR40 and GAPDH levels in the hypothalamus after CFA injection with or without flavopiridol are shown (B). White, black and grey bars represent saline, CFA and CFA+flavopiridol-injection groups, respectively. Mechanical allodynia was evaluated using von Frey filaments (C). Thermal hyperalgesia of the hind paw was assessed using the plantar test (D). Data, mean ± S.E.M.; Saline (n = 6), CFA (Day 7) (n = 6), CFA (Day 7)+flavopiridol 5 nmol (n = 6), CFA (Day 7)+flavopiridol 15 nmol (n = 6); ^#<i>p</i><0.05, ^##<i>p</i><0.01, compared with saline; *<i>p</i><0.05, compared with CFA (Scheffe's test).</p

Changes in hypothalamic GPR40 expression in CFA-induced inflammatory chronic pain mouse model.

<p>White bar, saline-injection group; black bar, CFA-injection group; data, mean ± S.E.M.; Saline (n = 6), CFA (Day 1) (n = 6), CFA (Day 3) (n = 6), CFA (Day 7) (n = 6), CFA (Day 14) (n = 6); and ^##<i>p</i><0.01, compared with saline (Student's <i>t</i>-test).</p