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PubMed2004

Relation between laminectomy and development of adjacent segment instability after lumbar fusion with pedicle fixation.

STUDY DESIGN: A retrospective study of 101 patients who had undergone posterolateral lumbar fusion, to analyze the association between adjacent instability and the extent of laminectomy. OBJECTIVES: To investigate the hypothesis that the integrity of the posterior complex (spinous process/supraspinous ligament/spinous process) between the fused segments and the neighboring motion segments significantly influences lumbar spine stability. SUMMARY OF BACKGROUND DATA: Spinal fusion with pedicle fixation accelerates the degeneration of adjacent motion segments. The lowest cranial motion segment is the most common level for the development of adjacent instability. Laminectomy, including removal of the spinous process, supraspinous ligament, interspinous ligament, lamina and ligamentum flavum, jeopardizes the integrity of the posterior complex of the spine. METHODS: This study enrolled 101 patients, followed up for at least 6 years, who had been treated with posterolateral lumbar fusion with pedicle fixation because of lumbar spondylolisthesis. The diagnosis of adjacent instability depended on the dynamic lateral views of the lumbosacral spine during each follow-up. The integrity of the posterior complex was based on the extent of laminectomy and the fusion level. RESULTS: At the cranial adjacent motion segment, 2 of 31 (6.5%) patients with preserved posterior complex integrity between the fused segment and motion segment developed adjacent instability, compared with 17 of 70 (24.3%) without preserved posterior complex integrity. At the caudal adjacent motion segment, none of 13 patients (0%) with preserved integrity developed adjacent instability, compared with 3 of 54 (5.6%) without preserved integrity. CONCLUSIONS: Damaging the integrity of the posterior complex between the fused segments and the neighboring motion segments may jeopardize lumbar spine stability. Sacrificing either the supraspinous ligament or the tendon insertion points on the spinous processes leads to an accelerated development of adjacent instability.

Adult↗
PubMed2005

Discogenic origins of spinal instability.

STUDY DESIGN: Cadaveric motion segment experiment. OBJECTIVE: To show how two physical aspects of disc degeneration (dehydration and endplate disruption) contribute to spinal instability. SUMMARY OF BACKGROUND DATA: The origins of spinal instability and its associations with back pain are uncertain. METHODS.: Twenty-one cadaveric thoracolumbar motion segments aged 48 to 90 years were secured in cups of dental plaster and loaded simultaneously in bending and compression to simulate full flexion, extension, and lateral bending movements. Vertebral movements, recorded using a two-dimensional "MacReflex" motion analysis system, were analyzed to calculate neutral zone (NZ), range of motion (ROM), bending stiffness (BS), horizontal translational movements, and the location of the center of rotation (COR). Intradiscal "stresses" were measured by pulling a miniature pressure transducer through the disc along its midsagittal diameter. All experiments were repeated after each of two treatments, which simulated physical aspects of disc degeneration: creep loading to dehydrate the disc and compressive overload to disrupt the endplate. Results were analyzed using ANOVA and linear regression. RESULTS: Motion segment height was reduced by 1.0 (SD 0.3) mm during creep and by a further 1.7 (0.6) mm after endplate disruption. In flexion and lateral bending, the combined treatments increased NZ and ROM by 89% to 298%, and increased the "instability index" (NZ/ROM) by 43% to 61%. Translational movements increased by 58% to 86%, whereas BS decreased by 42% to 48%. In extension, ROM and NZ were little affected, although the COR moved closer to the apophyseal joints. Measures of instability increased most in lateral bending, and following endplate disruption. Stress concentrations in the posterior anulus fibrosus increased markedly after endplate disruption. CONCLUSIONS: Two physical aspects of disc degeneration (dehydration and endplate disruption) cause marked segmental instability. Back pain associated with instability may be attributable to stress concentrations in degenerated discs.

Aged↗
PubMed2004

Activated oncogenes promote and cooperate with chromosomal instability for neoplastic transformation.

Most cancer cells are aneuploid. The chromosomal instability hypothesis contends that aneuploidy is the catalyst for transformation, whereas the gene mutation hypothesis asserts that cancer is driven by mutations to proto-oncogenes and tumor-suppressor genes, with the aneuploidy a side effect of tumorigenesis. Because genotoxic stress induced by "culture shock" can obscure the transforming potential of exogenous genes, we cultured wild-type and p53(-/-) mouse embryo fibroblasts in a more physiological (serum-free) environment. Under these conditions, the cells were immortal and, more importantly, chromosomally stable. Expression of oncogenic H-RasV12 did not induce senescence, but sensitized these cells to p53-dependent apoptosis. In addition, H-RasV12 induced chromosomal instability, as well as accumulation and phosphorylation of p53. Significantly, whereas cells grown under standard conditions could be transformed by coexpression of H-RasV12 and E1A, the chromosomally stable cells were refractory to transformation, as measured by anchorage-independent growth and tumor formation in nude mice. These oncogenes required a third genetic alteration that abolished the p53 pathway to create a permissive environment that promotes rapid chromosomal instability and transformation. Oncogene-induced chromosomal instability and transformation was attenuated by antioxidants. These data indicate that chromosomal instability could be a catalyst for oncogenic transformation, and bring together aspects of the chromosomal instability hypothesis and the gene mutation hypothesis for tumorigenesis.

Acetylcysteine↗
PubMed2006

Genetic instability on chromosome 17 in the epithelium of non-polypoid colorectal carcinomas compared to polypoid lesions.

Early colorectal carcinomas (submucosal invasive adenocarcinomas) can be classified into polypoid growth carcinoma (PG-Ca) and non-polypoid growth carcinoma (NPG-Ca) types, the latter transforming more rapidly to advanced carcinoma. Previously, we indicated that stromal genetic instability might contribute to tumorigenesis of both sporadic and ulcerative colitis-associated colorectal adenocarcinomas. In the present study, we analyzed genetic instability of both epithelial and surrounding stromal components in PG-Ca and NPG-Ca. In 99 colorectal submucosal invasive adenocarcinomas, epithelial and stromal genetic instability was analyzed with National Cancer Institute standard microsatellite markers, chromosome 17 (Chr.17) markers and tumor suppressor gene-related markers, using a combination of the laser-captured microdissection and GeneScan approaches. Immunohistochemical analysis was carried out for hMLH1, hMSH2, MGMT and p53. In addition, we investigated methylation of the hMLH1 and MGMT promoters. The frequencies of epithelial microsatellite instability (MSI) with Chr.17 markers were significantly higher in NPG-Ca (33.3%) compared to PG-Ca (10.4%), particularly with D17S579 and D17S796. For loss of heterozygosity, only D17S786 showed a significant difference. The frequencies of stromal MSI with all markers were 31.7% and 25.9% in NPG-Ca and PG-Ca, respectively, but D17S579 and TP53 showed higher MSI in NPG-Ca than PG-Ca. Immunohistochemically, p53 protein expression in PG-Ca was significantly higher in loss of heterozygosity-positive cases with altered Chr.17 markers overall, especially the D17S796 marker, compared to cases without genetic instability. These results suggest that epithelial and stromal MSI of Chr.17 markers contributes more to carcinogenesis in NPG-Ca, whereas stromal genetic instability might be necessary for the development of both types of colorectal carcinoma.

Adaptor Proteins, Signal Transducing↗
PubMedDate not supplied

Measurement of angles of abduction for diagnosis of shoulder instability in dogs using goniometry and digital image analysis.

OBJECTIVE: To compare abduction angles of shoulders with medial instability and unaffected shoulders in the same dogs and in age- and breed-matched dogs. STUDY DESIGN: Case-control study. ANIMALS: Dogs with medial instability of the shoulder (n=33) and 26 control dogs. METHODS: Dogs were sedated and positioned in lateral recumbency with both scapulas parallel to the table. With the elbow and shoulder in extension, the non-recumbent limb was maximally abducted and the angle between the scapular spine and lateral aspect of the brachium measured with a goniometer; a digital image was taken from the cranial aspect. Both techniques were performed in triplicate by 2 examiners. Mean abduction angles for each shoulder were determined from goniometric measurements and image analysis. Data were analyzed for significant differences between affected and unaffected shoulders, measurement techniques, and examiners. Strength of correlation between measurement techniques was determined. RESULTS: Mean abduction angles for shoulders with instability (53.7+/-4.7 degrees goniometric, 51.2+/-4.9 degrees image) were significantly (P<.001) larger than for all unaffected shoulders (32.6+/-2.0 degrees goniometric, 30.9+/-2.3 degrees image). In dogs diagnosed with instability, affected shoulders had significantly (P<.001) larger abduction angles than the contralateral (unaffected) shoulders. No significant differences were identified between right and left shoulders for control dogs, measurement techniques, or examiners. A strong (r=0.90) significant (P<.001) positive correlation between measurement techniques was noted. CONCLUSIONS: Shoulder abduction angles measured under sedation provide objective data for diagnosis of shoulder instability in dogs. Shoulders with clinical and arthroscopic evidence of medial instability have significantly higher abduction angles than shoulders that are considered normal. CLINICAL RELEVANCE: Determination of shoulder abduction angles should be included in the diagnostic protocol for forelimb lameness assessment in dogs.

Animals↗
PubMed2005

Epithelial and stromal genetic instability contributes to genesis of colorectal adenomas.

BACKGROUND: Previously, we indicated that stromal genetic instability might contribute to tumorigenesis of both sporadic and ulcerative colitis associated colorectal adenocarcinomas. Considering the established adenoma-adenocarcinoma sequence, in this study we analysed genetic instability in colorectal adenoma cells and surrounding stroma. METHODS: In 164 colorectal tumours (34 hyperplastic polyps, 38 tubular adenomas with low grade dysplasia (TA-L), 51 tubular adenomas with high grade dysplasia (TA-H), and 41 invasive carcinomas), epithelial and stromal genetic instability with National Cancer Institute standard microsatellite markers and chromosome 17 (Chr17) markers, were analysed by a combination of laser capture microdissection and GeneScan approaches. RESULTS: While frequencies of both loss of heterozygosity (LOH) and microsatellite instability (MSI) were extremely low in hyperplastic polyps, LOH in tubular adenomas was detected in both epithelial (TA-L 13.2%, TA-H 27.5%) and stromal (5.3% and 5.9%, respectively) elements, along with MSI (5.3% and 13.7%, and 5.3 and 5.9%, respectively). Frequencies of epithelial alterations were higher in TA-H than in TA-L, and greatest in the carcinoma group. On the other hand, frequencies of stromal LOH or MSI were almost constant (5.3% approximately 17.1%, 5.3% approximately 17.1%, respectively) in adenomas and invasive carcinomas. In addition, p53 was found to be significantly overexpressed in a greater proportion of TA-L with LOH than in those without genetic instability. CONCLUSION: The results indicate the presence of genetic alterations in stroma from an early stage of carcinogenesis, accompanied by stepwise increasing genetic instability of epithelia with progression to cancer. Thus microenvironmental changes due to genetic alteration in Chr17 markers in stromal cells may play an important role in colon adenoma and adenocarcinoma development.

Adenocarcinoma↗
PubMed2006

Chromosomal instability correlates with genome-wide DNA demethylation in human primary colorectal cancers.

DNA hypomethylation is a common trait of colorectal cancer. Studies in tumor cell lines and animal models indicate that genome-wide demethylation may cause genetic instability and hence facilitate or accelerate tumor progression. Recent studies have shown that DNA hypomethylation precedes genomic damage in human gastrointestinal cancer, but the nature of this damage has not been clearly established. Here, we show a thorough analysis of DNA methylation and genetic alterations in two series of colorectal carcinomas. The extent of DNA demethylation but not of hypermethylation (both analyzed by amplification of intermethylated sites in near 200 independent sequences arbitrarily selected) correlated with the cumulated genomic damage assessed by two different techniques (arbitrarily primed PCR and comparative genomic hybridization). DNA hypomethylation-related instability was mainly of chromosomal nature and could be explained by a genome-wide effect rather than by the concurrence of the most prevalent genetic and epigenetic alterations. Moreover, the association of p53 mutations with genomic instability was secondary to DNA hypomethylation and the correlation between DNA hypomethylation and genomic instability was observed in tumors with and without mutation in the p53 gene. Our data support a direct link between genome-wide demethylation and chromosomal instability in human colorectal carcinogenesis and are consistent with the studies in model systems demonstrating a role of DNA demethylation in inducing chromosomal instability.

Chromosomal Instability↗
PubMedDate not supplied

Arthroscopic laser-assisted capsular shift in the treatment of patients with multidirectional shoulder instability.

BACKGROUND: In recent years, various investigators have begun using lasers in the treatment of shoulder instability. HYPOTHESIS: Arthroscopic laser-assisted capsular shift is an effective treatment for patients with multidirectional shoulder instability. STUDY DESIGN: Retrospective cohort study. METHODS: We retrospectively identified 28 patients (30 shoulders) with multidirectional shoulder instability who were unresponsive to nonoperative management and who had undergone the laser-assisted capsular shift procedure. Twenty-five patients (27 shoulders) with an average follow-up of 28 months were available for review. All patients underwent a physical examination and completed a general questionnaire; the University of California, Los Angeles, shoulder rating scale; the Western Ontario Shoulder Instability Index; and the Short-Form 36 quality of life index. RESULTS: In 22 shoulders, results of the procedure were considered a success because the patients had no recurrent symptoms and at latest follow-up had required no further operative intervention. In five shoulders, results were considered a failure because of recurrent pain or instability and the need for an open capsular shift procedure. With recurrent instability as a measure of failure, the overall success rate was 81.5%. CONCLUSIONS: Our results with laser-assisted capsular shift are comparable with the results of other open and arthroscopic techniques in relieving pain and returning athletes to their premorbid function.

Adolescent↗
PubMedDate not supplied

Arthroscopic capsulolabroplasty for posteroinferior multidirectional instability of the shoulder.

BACKGROUND: Arthroscopic treatment of posteroinferior multidirectional instability of the shoulder is not well documented. PURPOSE: To evaluate pathologic lesions of posteroinferior multidirectional instability and the results of arthroscopic capsulolabroplasty. STUDY DESIGN: Prospective nonrandomized clinical trial. METHODS: Thirty-one patients with posteroinferior multidirectional instability were prospectively evaluated after arthroscopic capsulolabroplasty (mean follow-up, 51 months). Labral lesion and height were measured in the MRI arthrogram and arthroscopic examination. RESULTS: All patients had a labral lesion and variable capsular stretching in the posteroinferior aspect. There were 11 type I labral lesions (incomplete detachment), 12 type II (the Kim's lesion: incomplete and concealed avulsion), 6 type III (chondrolabral erosion), and 2 type IV (flap tear). All patients with type II and III lesions had chondrolabral retroversion, with lost labral height in the MRI arthrogram and arthroscopic examination. Twenty-one patients had an excellent Rowe score, nine had good scores, and one had a fair score. Thirty patients had stable shoulders, and one had recurrent instability. All patients had improved shoulder scores and function and pain scores. CONCLUSIONS: Symptomatic patients with posteroinferior multidirectional instability had posteroinferior labral lesions, including retroversion of the posteroinferior labrum, which were previously unrecognized. Restoration of the labral buttress and capsular tension by arthroscopic capsulolabroplasty successfully stabilized shoulders with posteroinferior multidirectional instability.

Adult↗
PubMed2005

Peroneus longus muscle activation pattern during gait cycle in athletes affected by functional ankle instability: a surface electromyographic study.

BACKGROUND: Functional ankle instability is a clinical syndrome that may develop after acute lateral ankle sprain. Although several causes of this functional instability have been suggested, it is still unclear what the activation pattern of the peroneus longus muscle is in patients with functional ankle instability. HYPOTHESIS: Peroneus longus activation patterns differ in the injured side and the uninjured side in subjects with functional ankle instability. STUDY DESIGN: Descriptive laboratory study. METHODS: The authors examined 14 subjects with functional ankle instability by using surface electromyography during walking. Activation time of the peroneus longus muscle was expressed as a percentage of the stance phase of the gait cycle. RESULTS: A statistically significant decrease in peroneus longus muscle activity was found in the injured side compared with the uninjured side (22.8% +/- 4.25% vs 37.6% +/- 3.5%, respectively). CONCLUSIONS: Results obtained in this study show a change in peroneus longus muscle activation time after injury. Independent of the origin of this change, which could only be surmised, the decrease in peroneus longus muscle activity may result in reduced protection against lateral sprains. CLINICAL RELEVANCE: The assessment of peroneus longus activation pattern during gait is useful to design an appropriate rehabilitation program in athletes suffering from functional ankle instability.

Adolescent↗
PubMed2006

An in vivo injury model of posterolateral knee instability.

BACKGROUND: Posterolateral knee instability is a difficult clinical problem to diagnose and treat. To best evaluate its natural history and the effects of interventional treatments, it is important to develop an in vivo model in an attempt to validate human cadaveric and clinical observational studies. PURPOSE: To develop an in vivo model of posterolateral knee instability in the rabbit and to determine the natural history of untreated posterolateral knee injuries at 6 months postoperatively. STUDY DESIGN: Controlled laboratory study. METHODS: The fibular collateral ligament and popliteus tendon were surgically transected in 1 knee in each of 10 skeletally mature New Zealand White rabbits, with the contralateral knee serving as a control knee. At 6 months postoperatively, the rabbits were euthanized, the knees were removed, and biomechanical testing of knee joint stability was performed. After biomechanical testing, histological sections of each proximal tibia and distal femur were evaluated, and each proximal tibia was graded using an osteoarthritis grading scheme. RESULTS: Biomechanical testing revealed a statistically significant difference in amount of rotation in the operated knees compared with the unoperated control knees to varus moments at 30 degrees , 60 degrees , and 90 degrees and to external rotation torques at 30 degrees and 60 degrees . Morphological analysis revealed no significant difference in lesions of osteoarthritis in the medial compartment of the operated knees compared with the unoperated knees. CONCLUSIONS: Although the presence of posterolateral knee instability was validated 6 months after surgery in this model, the authors did not identify significant differences in lesions of osteoarthritis in the operated knees compared with the unoperated control knees. CLINICAL SIGNIFICANCE: This study confirms that posterolateral knee instability can be created in an animal model. It also recapitulates the clinical observation in humans that untreated posterolateral knee injuries do not heal. Similar to animal models of medial collateral ligament sectioning, further studies to validate a posterolateral instability knee model may lead to interventional studies to determine the best way to treat this complex knee instability pattern.

Animals↗
PubMedDate not supplied

Patterns of flexibility, laxity, and strength in normal shoulders and shoulders with instability and impingement.

Imbalance of the internal and external rotator musculature of the shoulder, excess capsular laxity, and loss of capsular flexibility, have all been implicated as etiologic factors in glenohumeral instability and impingement syndrome; however, these assertions are based largely on qualitative clinical observations. In order to quantitatively define the requirements of adequate protective synergy of the internal and external rotator musculature, as well as the primary capsulolabral restraints, we prospectively evaluated 53 subjects: 15 asymptomatic volunteers, 28 patients with glenohumeral instability, and 10 patients with impingement syndrome. Range of motion was evaluated by goniometric technique in all patients with glenohumeral instability and impingement. Laxity assessment was performed and anterior, posterior, and inferior humeral head translation was graded on a scale of 0 to 3+. Isokinetic strength assessment was performed in a modified abducted position using the Biodex Clinical Data Station with test speeds of 90 and 180 deg/sec. Internal and external rotator ratios and internal and external rotator strength deficits were calculated for both peak torque and total work. Patients with impingement demonstrated marked limitation of shoulder motion and minimal laxity on drawer testing. Both anterior and multidirectional instability patients had excessive external rotation as well as increased capsular laxity in all directions. Sixty-eight percent of the patients with instability had significant impingement signs in addition to apprehension and capsular laxity. Isokinetic testing of asymptomatic subjects demonstrated a 30% greater internal rotator strength in the dominant shoulder. Comparison of all three experimental groups demonstrated a significant difference between internal and external rotator ratios for both peak torque and total work. Conclusions are that there appears to be a dominance tendency with regard to internal rotator strength in asymptomatic individuals. Impingement syndrome and anterior instability have significant differences in both strength patterns of the rotator muscles and flexibility and laxity of the shoulder. Isokinetic testing potentially may be helpful in diagnostically differentiating between these two groups in cases where there is clinical overlap of signs and symptoms.

Adult↗
PubMed2005

Genomic instability in human lymphocytes irradiated with individual charged particles: involvement of tumor necrosis factor alpha in irradiated cells but not bystander cells.

Exposure to ionizing radiation can increase the risk of cancer, which is often characterized by genomic instability. In environmental exposures to high-LET radiation (e.g. 222Ra), it is unlikely that many cells will be traversed or that any cell will be traversed by more than one alpha particle, resulting in an in vivo bystander situation, potentially involving inflammation. Here primary human lymphocytes were irradiated with precise numbers of 3He2+ ions delivered to defined cell population fractions, to as low as a single cell being traversed, resembling in vivo conditions. Also, we assessed the contribution to genomic instability of the pro-inflammatory cytokine tumor necrosis factor alpha (TNFA). Genomic instability was significantly elevated in irradiated groups (> or = two-fold over controls) and was comparable whether cells were traversed by one or two 3He2+ ions. Interestingly, substantial heterogeneity in genomic instability between experiments was observed when only one cell was traversed. Genomic instability was significantly reduced (60%) in cultures in which all cells were irradiated in the presence of TNFA antibody, but not when fractions were irradiated under the same conditions, suggesting that TNFA may have a role in the initiation of genomic instability in irradiated cells but not bystander cells. These results have implications for low-dose exposure risks and cancer.

Bystander Effect↗
PubMed1993

Instability of the shoulder after arthroplasty.

A replacement arthroplasty was performed in 236 shoulders at The Hospital for Special Surgery from 1984 through 1989. Ten patients (eight women and two men) from that group were identified as having instability of the shoulder at the time of follow-up, and the results for these patients were reviewed retrospectively. The ages of the patients ranged from fifty-six to seventy-nine years. The instability was anterior in seven of the patients and posterior in three. The anterior instability was caused by a rupture of the repaired subscapularis tendon. The operative treatment of the anterior instability consisted of mobilization and repair of the tendon, but three of the seven patients continued to have instability. A static stabilizer, consisting of an allograft of Achilles tendon, was inserted in these three patients, and the result was a success. The etiology of the posterior instability (three patients) was multifactorial. Treatment consisted of correction of any soft-tissue imbalance and revision of the prosthetic components as necessary. All ten patients were followed clinically and radiographically for at least two years. All of the patients had some loss of motion of the shoulder as compared with the motion before the dislocation. There were no neurovascular complications, problems related to the allografts, or any other complications. We concluded that proper balancing of the soft tissues and positioning of the prosthetic components are essential to a successful arthroplasty of the shoulder. The postoperative rehabilitation should include a physical therapy program in which the range of motion of the arm that was achieved in the operating room is not exceeded.(ABSTRACT TRUNCATED AT 250 WORDS)

Achilles Tendon↗
PubMed2001

Tardy posterolateral rotatory instability of the elbow due to cubitus varus.

BACKGROUND: Cubitus varus has long been considered merely a cosmetic deformity. The purpose of this paper is to demonstrate a causal relationship between cubitus varus and instability of the elbow. METHODS: In twenty-four patients (twenty-five limbs) with a cubitus varus deformity following a pediatric distal humeral fracture or resulting from a congenital anomaly (three limbs of two patients), tardy posterolateral rotatory instability of the elbow developed approximately two to three decades after the deformity occurred. All patients presented with lateral elbow pain and recurrent instability. The average varus deformity was 15 degrees (range, 0 degrees to 35 degrees ). Surgery was performed in twenty-one patients (twenty-two limbs). Treatment consisted of reconstruction of the lateral collateral ligament and osteotomy in seven limbs, ligament reconstruction alone in ten, osteotomy alone in four, and total elbow arthroplasty in one. RESULTS: In three patients, the triceps muscle was dynamically stimulated intraoperatively to contract while resisting extension of the elbow. This produced posterolateral rotatory subluxation of the elbow, which was reversed by corrective osteotomy and lateral transposition of a portion of the medial head of the triceps that originally had been attached to the elongated, deformed medial aspect of the olecranon. At an average of three years (minimum, one year) after the operation, the result was good or excellent for nineteen of the twenty-two limbs that had undergone an operation; three limbs had persistent instability. CONCLUSIONS: With cubitus varus, the mechanical axis, the olecranon, and the triceps line of pull are all displaced medially. The repetitive external rotation torque on the ulna permitted by these deformities can stretch the lateral collateral ligament complex and lead to posterolateral rotatory instability. Thus, cubitus varus deformity secondary to supracondylar malunion or congenital deformity of the distal part of the humerus may not always be a benign condition and may have important long-term clinical implications. Operative correction can relieve symptoms of instability. The indications for preventive corrective osteotomy remain to be determined.

Adolescent↗
PubMed2005

Reliability, validity, and responsiveness of the American Shoulder and Elbow Surgeons subjective shoulder scale in patients with shoulder instability, rotator cuff disease, and glenohumeral arthritis.

BACKGROUND: Outcomes assessment after the treatment of shoulder disorders has involved the use of various condition-specific outcome instruments. The purpose of this study was to determine the psychometric properties of the American Shoulder and Elbow Surgeons subjective shoulder scale in patients with shoulder instability, rotator cuff disease, and glenohumeral arthritis. METHODS: Test-retest reliability, internal consistency, content validity, criterion validity, construct validity, and responsiveness to change were determined for the American Shoulder and Elbow Surgeons shoulder scale within subsets of an overall study population of 455 patients with shoulder instability, 474 patients with rotator cuff disease, and 137 patients with glenohumeral arthritis. RESULTS: There was acceptable test-retest reliability for the overall American Shoulder and Elbow Surgeons shoulder scale (intraclass correlation coefficient = 0.94) and ten of eleven domains. There was acceptable internal consistency for patients with instability (Cronbach alpha = 0.61), rotator cuff disease (0.64), and arthritis (0.62). There were acceptable floor and ceiling effects for patients with instability (0% and 1.3%, respectively), rotator cuff disease (0% for both), and arthritis (0% for both). There was acceptable and appropriate criterion validity, with significant correlations (p < 0.05) between the overall American Shoulder and Elbow Surgeons scale and the physical functioning, role-physical, and bodily pain domains of the Short Form-12 scale, and nonsignificant correlations (p > 0.05) with the role-emotional, mental health, vitality, and social function domains. There was acceptable construct validity, with all twenty-three hypotheses demonstrating significance (p < 0.05), and acceptable responsiveness to change for patients with instability (standardized response mean, 0.93), rotator cuff disease (1.16), and arthritis (1.11). CONCLUSIONS: The use of outcome instruments with psychometric properties that have been vigorously established is essential. The American Shoulder and Elbow Surgeons subjective shoulder scale demonstrated overall acceptable psychometric performance for outcomes assessment in patients with shoulder instability, rotator cuff disease, and glenohumeral arthritis.

Adolescent↗
PubMed1998

Is exposure to environmental or industrial endocrine disrupting estrogen-like chemicals able to cause genomic instability?

Human and wild life populations are continually exposed to a wide variety of environmental estrogen-like chemicals. Most research to date on environmental endocrine disrupting estrogen-like chemicals has focussed on screening of estrogenic activity of environmental or industrial chemicals, their bioaccumulative properties and toxicokinetics, and developing the structure-activity relationship between environmental or industrial chemicals and estrogen-receptor. Whether estrogen-like chemicals also possess the ability to alter the stability of the genome is not clear. It is very important to understand the effects of estrogen-like chemicals at the genome level. This article evaluates the current status of knowledge of the potential of producing genomic instability in response to the exposure of estrogen-like chemicals, which might help in understanding the mechanisms of some of the adverse effects. We and others have shown several structural, numerical, and functional changes at the cellular levels in response to DES exposure. Some other phenolic estrogen-like chemicals, such as, bisphenol A, phenylphenol and nonylphenol, also follow some of the pattern of effects similar to DES. These compounds also alter cell cycle kinetics, induce DNA damages, and produce telomeric associations and chromosomal aberrations. Whether weak or strong, the estrogenic response of a chemical, if not overcome, will add extra estrogenic burden to the system, and particularly those endocrine disrupting environmental and industrial estrogen-like chemicals capable of producing genomic instability will induce additional burden of genomic instability. Though, estrogenically some of these compounds may be weak, however, they may have different activities in generation of genomic instability. For example, nonylphenol is weak in estrogen-like action compared to DES, however, it is equal or more potent in producing telomeric associations in MCF-7 cells compared to DES. Additive or synergistic extra-burden of estrogenicity and genomic instability could produce detrimental effects compare to estrogenic action alone. Screening of endocrine disrupting environmental estrogen-like chemicals for their ability to produce genomic instability and analysis of molecular basis of some of the adverse human health outcomes as a result of exposure of these types of chemicals should lead to a better understanding of how these environmental estrogen-like chemicals may influence the development of some adverse effects in humans and wildlife.

Animals↗
PubMed2006

Morphometric and qualitative analysis of congenital occipitocervical instability in children: implications for patients with Down syndrome.

OBJECT: Congenital occipitocervical (OC) instability is uncommon in healthy children but can occur in many children with Down syndrome. A simple morphometric method of evaluating the OC joint in children with OC instability is presented, supported by a qualitative image analysis based on computed tomography (CT). METHODS: Thin-cut CT scans of the OC joint were obtained in eight patients with Down syndrome and one patient with congenital OC instability. These patients' CT scans were compared with those of 15 healthy age-matched control individuals. Morphometric analysis was performed by measuring the depth and length of the superior articular surface (SAS) of C-1, and these values were normalized for a comparison between groups. Qualitative data were acquired using a surface-rendering technique for a visual comparison of the C-1 SAS. Morphometric analysis demonstrated an absence of the concave C-1 SAS anatomy in patients with congenital OC instability compared with age-matched control individuals (0.083 compared with 0.202, p < 0.001). Three-dimensional (3D) image analysis of the C-l SAS supported this finding. CONCLUSIONS: Congenital differences in the shape of the OC joint are highly associated with atraumatic OC instability in children with Down syndrome. High-resolution CT imaging combined with 3D rendering techniques and surface mapping provides support for this assessment. It appears that abnormal OC joint shape is a contributing factor to congenital OC instability, especially in patients with Down syndrome.

Adolescent↗