Hyper extension-internal rotation (HERI): A new test for anterior gleno-humeral instability.

BACKGROUND: Anterior shoulder dislocation causes injury to the inferior gleno-humeral ligament (IGHL) and capsule. Clinical manoeuvres currently used to evaluate the IGHL test for, and may induce, apprehension. We developed the hyper extension-internal rotation (HERI) test to assess the IGHL and inferior capsule without causing apprehension or inducing a risk of gleno-humeral dislocation. HYPOTHESIS: The HERI test is easy to perform and reproducible, induces no risk of gleno-humeral dislocation during the manoeuvre, and causes no apprehension in the patients. MATERIAL AND METHODS: We studied 14 fresh cadaver shoulders. Each specimen was positioned supine with the lateral edge of the scapula on the table and the upper limb hanging down beside the table under the effect of gravity. This position produced hyperextension and internal rotation of the gleno-humeral joint. For each shoulder, the range of extension (°) was measured before and after isolated IGHL section. Then, we performed the HEIR test in 50 patients with chronic unilateral anterior gleno-humeral instability and we compared the range of extension between the normal and abnormal sides. RESULTS: In the cadaver study, isolated IGHL section increased the angle of extension by a mean of 14.5° (11°-18°) compared to the pre-injury values. In the clinical study, the mean difference in extension angles between the normal and abnormal sides was 14.5°. The patients reported no apprehension during the HERI test. CONCLUSION: The angle of extension increases after section or injury of the IGHL in cadaver specimens and patients, respectively. When the inferior capsule and IGHL are damaged, the angle of extension increases compared to the normal side. Lesions to these structures can be evaluated clinically by performing the HERI test. LEVEL OF EVIDENCE: III.

Results of surgical treatment of calcaneus insertional tendinopathy in middle- and long-distance runners.

PURPOSE: Calcaneus insertional tendinopathy in runners is common and involves important therapeutic controversies. The object of this study was to determine the delay and level of return to sport after insertional surgery in runners, with and without tendon damage. METHODS: Eighteen runners underwent surgery for insertional calcaneus tendinopathy. Nine required an exostosectomy/bursectomy, and nine others required a tendon reinsertion/autograft. All patients were clinically assessed pre- and post-operatively with AOFAS scores and post-operatively with ATRS. This series included analysis of "pure conflicts" and "severe insertional lesion" scores. If the insertional tendon was free or the lesion was smaller than 50 %, the group was classified as "pure conflict/minor tendon damage". In the situation in which a loss of tendon occurred or the tendon lesion was greater than 50 %, the group was classified as "major tendon damage". Pre-operatively, the AOFAS "overall", "pure conflicts/minor tendon damage" and "major tendon damage" groups' scores were 58.5 ± 15, 68.2 ± 8.8 and 48.9 ± 13.9/100, respectively. RESULTS: Post-operatively, the AOFAS "overall", "pure conflicts/minor tendon" and "major tendon damage" groups' scores were 93.7 ± 8.2, 93.2 ± 10.2 and 95.2 ± 5.7/100, respectively. The AOFAS score gain for each group was, respectively, 35.2 ± 19, 24 ± 17 and 46.3 ± 14.1. The ATRS "overall", "pure conflicts/minor tendon damage" and "major tendon damage" groups' scores were 81.5 ± 14.9, 78.3 ± 20.1 and 84.7 ± 6.7/100, respectively. The global sport recovery delay was 9.3 ± 4.1 months; it was 6 ± 3.3 months for the pure conflict/minor tendon damage subgroup and 10 ± 4.6 months for the severe tendon damages subgroup. CONCLUSION: Achilles insertional tendinopathy surgery on this population results in few complications with good functional results if the surgical technique is adapted to the type of tendon injury. The clinical relevance of this study is that it highlights the various forms of calcaneus insertional tendinopathy and various treatment options. The authors show that in the case of major tendon damage, time to return to sport is longer.

Purification and physical-chemical characterization of hepatic stimulator substance.

Hepatic stimulator substance is a liver growth stimulator derived from the hepatocyte cytosol of weanling or regenerating adult rat livers. The present paper reports the almost 9,000-fold purification of hepatic stimulator substance with an approximately 100,000-fold increase in specific growth stimulator activity. Purification steps included heating at 95 degrees C for 15 min, 40% cold ethanol precipitation, passage over Procion Red HE3B, DEAE cellulose and Sephadex G75 columns and gel filtration and reverse-phase fast protein liquid chromatography techniques. As little as 27 ng per ml of the purest material produced a 2-fold stimulation in the standard HTC cell activity assay. Further studies indicate that hepatic stimulator substance is a highly negatively charged protein and that disulfide bonds or a complex tertiary structure are not essential to its activity. Hepatic stimulator substance is stable over a wide range of pH's and temperatures. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis with silver stain revealed 1 major band at 12,400 daltons and 1 minor band at 17,500 daltons.

Stimulation of HTC hepatoma cell growth in vitro by hepatic stimulator substance (HSS). Interactions with serum, insulin, glucagon, epidermal growth factor and platelet derived growth factor.

Hepatic stimulator substance (HSS), a partially purified extract of weanling or regenerating adult rat liver, is an organ-specific stimulator of liver growth in vivo and in vitro. The HTC hepatoma cell line is particularly responsive to HSS. The present experiments show that HSS will stimulate HTC cells in the complete absence of serum, although graded doses of fetal cal serum (FCS), from 0.1 to 5.0%, will increase the degree of stimulation in a dose-dependent manner. In contrast, when HSS is absent, increasing doses of FCS above 0.5% inhibit DNA synthesis. Much of this inhibition is removed by prior dialysis of the FCS and maximum enhancement of the HSS-induced stimulation occurs with only 0.1-0.5% of the dialysed FCS. Sera from older animals have less or even negative effect. Evidence is presented to show that the enhanced stimulation by HSS in the presence of serum is not due to insulin, glucagon, epidermal growth factor (EGF), or platelet derived growth factor (PDGF) and that HSS does not act via a shared receptor for one of these hormones. These experiments provide further evidence that HSS is a unique stimulator of liver growth and lend support to a model of organ-specific growth control.