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At least 127 records · Page 7Linked to original sources
PubMed1997

Microsatellite instability in colorectal adenomas.

BACKGROUND & AIMS: Microsatellite instability in apparently sporadic, predominantly right-sided colon cancers seems to be the result of an acquired, rather than germline, genetic change that impairs mismatch repair. The timing of this change with respect to the adenomacarcinoma sequence has not been determined. The aim of this study was to evaluate colonic adenomatous polyps for microsatellite instability to determine whether instability reflects an early genetic change in colonic neoplasia. METHODS: Ninety-three sporadic colonic adenomas (44 right-sided and 49 left-sided) from 48 individuals were evaluated for microsatellite instability with a set of 10 polymerase chain reaction primer sets. RESULTS: Eighty percent of adenomatous polyps showed no instability. Ninety-eight percent showed instability with <30% of primer sets. Aside from one right-sided adenoma with 78% instability, there was no level of instability with a higher proportion of right-sided than left-sided adenomas. CONCLUSIONS: Colonic adenomas show far less microsatellite instability than carcinomas, and the marked right-sided predominance of instability observed in colon cancers was not observed. Instability is usually not an early event in the development of colonic neoplasia. A distinct pathway to sporadic colorectal cancer initiated by mismatch repair deficiency, although not excluded, is not suggested by these data.

Adenoma↗
PubMed2002

Microsatellite instability in intraductal papillary neoplasms of the biliary tract.

Intraductal papillary neoplasms of the biliary tree are unusual lesions characterized by solitary or diffuse growth along the intra- and/or extrahepatic biliary tract. Biliary papillary neoplasms bear some clinicopathologic similarity to intraductal papillary mucinous neoplasms of the pancreas. Like intraductal papillary mucinous neoplasms of the pancreas, biliary papillary neoplasms can be purely intraductal lesions or can give rise to invasive adenocarcinomas. We recently studied the genetic alterations present in a series of biliary papillary neoplasms and noted the presence of allelic shifts in some biliary tumors during allelic loss assays on chromosomes 5q and 18q. This suggested that microsatellite instability might play a role in the molecular pathogenesis of biliary papillary neoplasms. Genomic DNA was extracted from 17 intraductal papillary neoplasms, 6 associated invasive cholangiocarcinomas, and corresponding normal tissues, and microsatellite instability testing was performed using the 5 microsatellite loci recommended by the 1997 National Cancer Institute-sponsored consensus conference (D2S123, D5S346, D17S250, Bat-25, and Bat-26). High-level microsatellite instability was considered to be present when at least two of five microsatellite loci showed allelic shifts, and low-level microsatellite instability, when only one locus was shifted, as per the National Cancer Institute criteria. We also determined the methylation status of the DNA mismatch repair gene hMLH1 by bisulfite treatment of genomic DNA, followed by methylation-specific PCR. High-level microsatellite instability was present in 2 of 17 (11.8%) biliary papillary neoplasms, including 1 case of purely intraductal tumor and 1 case with both intraductal and invasive cholangiocarcinoma components. In both cases there was extensive microsatellite instability, with allelic shifts in five of five and four of five microsatellite markers, respectively. Low-level microsatellite instability was present in 6 of 17 (35.3%) biliary papillary neoplasms, including 2 cases of purely intraductal tumor and 4 cases with both intraductal and invasive cholangiocarcinoma components. Interestingly, the pattern of allelic shifts was frequently not identical between the intraductal and invasive cholangiocarcinoma components; although the same microsatellite markers were shifted, alleles of differing lengths were generated in the intraductal and invasive components of the neoplasms with high-level microsatellite instability and of two neoplasms with low-level microsatellite instability. None of the biliary papillary neoplasms (0 of 10 cases with adequate DNA for evaluation) showed methylation of hMLH1. These results indicate that microsatellite instability is a relatively frequent event in papillary neoplasms of the biliary tree but is not associated with hMLH1 promoter hypermethylation. The finding that alleles of differing lengths were frequently generated between the intraductal and invasive components of those tumors with microsatellite instability suggests that there is significant genetic heterogeneity within these neoplasms.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Relativistic electromagnetic ion cyclotron instabilities.

The relativistic instabilities of electromagnetic ion cyclotron waves driven by MeV ions are analytically and numerically studied. As caused by wave magnetic field and in sharp contrast to the electrostatic case, interesting characteristics such as Alfve nic behavior and instability transition are discovered and illuminated in detail. The instabilities are reactive and are raised from the coupling of slow ions' first-order resonance and fast ions' second-order resonance, that is an essential extra mechanism due to relativistic effect. Because of the wave magnetic field, the nonresonant plasma dielectric is usually negative and large, that affects the instability conditions and scaling laws. A negative harmonic cyclotron frequency mismatch between the fast and slow ions is required for driving a cubic (and a coupled quadratic) instability; the cubic (square) root scaling of the peak growth rate makes the relativistic effect more important than classical mechanism, especially for low fast ion density and Lorentz factor being close to unity. For the cubic instability, there is a threshold (ceiling) on the slow ion temperature and density (the external magnetic field and the fast ion energy); the Alfve n velocity is required to be low. This Alfve nic behavior is interesting in physics and important for its applications. The case of fast protons in thermal deuterons is numerically studied and compared with the analytical results. When the slow ion temperature or density (the external magnetic field or the fast ion energy) is increased (reduced) to about twice (half) the threshold (ceiling), the same growth rate peak transits from the cubic instability to the coupled quadratic instability and a different cubic instability branch appears. The instability transition is an interesting new phenomenon for instability.

Journal Article↗
PubMed2006

Light-induced deformation and instability of a liquid interface. I. Statics.

We study in detail the deformations of a liquid-liquid interface induced by the electromagnetic radiation pressure of a focused cw laser beam. Using a simple linear model of static equilibrium of the interface under the effect of radiation pressure, buoyancy, and Laplace pressure, we explain the observed hump height variations for any value of the optical Bond number Bo=(omega0/lc)2 (lc is the capillary length and omega0 is the waist of the beam) in the regime of weak deformations and show that the deformations are independent of the direction of propagation of the laser. By increasing the beam power, we observe an instability of the interface leading to the formation of a long jet when the laser propagates from the more refringent phase to the less refringent one. We propose that the total internal reflection of the incident light on the highly deformed interface could be at the origin of this instability. Using a nonlinear model of static equilibrium of the interface taking account of the angular dependance of radiation pressure, we explain the measured beam power threshold of the instability P, as well as the shape of the interface deformations observed at large waists just below the instability onset. According to this model, the instability should occur when the interface slope reaches the angle of total reflection, theta(TR). We find experimentally that, just below the instability threshold, the maximum incidence angle along the interface, theta(imax), is significantly smaller than theta(TR) and that our nonlinear model does not present any instability up to theta(imax)=theta(TR). Thus, although the proposed instability model correctly predicts the instability threshold P, it fails to describe the actual instability mechanism. We finally discuss possible additional effects that could explain the instability.

Journal Article↗
PubMed1998

Telomerase activity and microsatellite instability in colorectal cancer and adenoma.

In order to examine their roles in carcinogenesis or in progression of colorectal carcinoma, we investigated telomerase activity and microsatellite instability in 67 non-familial colorectal cancers and in 18 adenomas. The incidence of detectable telomerase activity increased from 22% of normal colorectal mucosas adjacent to carcinoma, and 33% of adenomas, to 75% of carcinomas. On the other hand, the incidence of detectable microsatellite instability in carcinomas (30%) was almost the same as in adenomas (22%). No significant correlation was detected in the incidence of telomerase activity and microsatellite instability in carcinomas or in adenomas. Moreover, the incidence of telomerase activity and microsatellite instability did not increase during the progression of carcinomas. These results indicate that telomerase activity and microsatellite instability are independent events in colorectal carcinogenesis, and that telomerase activity and microsatellite instability are not correlated with the progression of colorectal carcinoma. However, in 13 multiple cancers, the incidence of telomerase activity (92%) and the incidence of microsatellite instability (54%) was higher than that of telomerase activity (70%) and that of microsatellite instability (24%) in 54 sporadic cancers. Moreover, the incidence of telomerase activity and that of microsatellite instability in adenomas with carcinomas (45% and 36% respectively) was higher than that of telomerase activity and microsatellite instability in adenomas without carcinomas (14% and 0% respectively). These results indicate that telomerase activity and microsatellite instability may play an important role in multicentric carcinogenesis in colorectal carcinoma.

Adenoma↗
PubMed1991

An anatomic basis for spinal instability: a porcine trauma model.

To determine the anatomic basis for spinal instabilities, 16 porcine cervical spine specimens were subjected to a well-defined sagittal plane trauma. The multidirectional instability of each specimen was measured before and after trauma. Detailed anatomic dissections were performed on each traumatized specimen to quantitate the extent of injury to several distinct anatomic structures and columns. Multiple regression models were constructed to determine which anatomic structures and columns correlated best with each multidirectional instability. Flexion instability correlated best with injury to the interspinous/supraspinous ligaments and the ligamentum flavum. Extension instability correlated best with anterior longitudinal ligament and pedicle injury. Axial rotation instability correlated best with anterior disc-end-plate and capsular ligament injuries, while lateral bending instability correlated best with posterior disc-end-plate injuries. Anterior column injuries correlated best with extension, axial rotation, and lateral bending instabilities, while posterior column injuries correlated best with flexion instability. Finally, individual anatomic structural injuries had higher correlations with multidirectional instabilities than did the injuries defined by the anatomic columns.

Animals↗
PubMed1984

Rotatory instability of cadaver knees after transection of collateral ligaments and capsule.

The importance of the medial and lateral compartment ligaments of the knee in relation to valgus-varus and axial rotation instability was investigated. Mobility patterns were drawn from 20 osteoligamentous knee preparations after successive transections of the structures. Cutting of the medial collateral ligament resulted only in slight valgus instability and modest anteromedial instability. When the medial posterior joint capsule was also cut, both types of instability increased, and moreover, the knee became posteromedially unstable. Cutting of the lateral collateral ligament produced only a little varus instability and anterolateral rotatory instability, but varus instability increased considerably when the posterior lateral capsule was also transected. In this latter situation, even marked posterolateral rotatory instability was found. Isolated transection of the medial or lateral collateral ligament did not cause any major valgus or varus instability, but when the posterior capsule was also transected, a considerable degree rotatory instability could be found even though the cruciate ligaments were intact.

Biomechanical Phenomena↗
PubMed2000

Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability.

OBJECTIVE: To assess the shape of the posterior glenoid rim in patients with recurrent (atraumatic) posterior instability. DESIGN AND PATIENTS: CT examinations of 15 shoulders with recurrent (atraumatic) posterior instability were reviewed in masked fashion with regard to abnormalities of the glenoid shape, specifically of its posterior rim. The glenoid version was also assessed. The findings were compared with the findings in 15 shoulders with recurrent anterior shoulder instability and 15 shoulders without instability. For all patients, surgical correlation was available. RESULTS: Fourteen of the 15 (93%) shoulders with recurrent (atraumatic) posterior shoulder instability had a deficiency of the posteroinferior glenoid rim. In patients with recurrent anterior instability or stable shoulders such deficiencies were less common (60% and 73%, respectively). The craniocaudal length of the deficiencies was largest in patients with posterior instability. When a posteroinferior deficiency with a craniocaudal length of 12 mm or more was defined as abnormal, sensitivity and specificity for diagnosing recurrent (atraumatic) posterior instability were 86.7% and 83.3%, respectively. There was a statistically significant difference in glenoid version between shoulders with posterior instability and stable shoulders (P=0.01). CONCLUSION: Recurrent (atraumatic) posterior shoulder instability should be considered in patients with a bony deficiency of the posteroinferior glenoid rim with a craniocaudal length of more than 12 mm.

Adolescent↗
PubMed2000

Posterior cruciate ligament and coupled posterolateral instability of the knee.

We wanted to investigate the role of the posterior cruciate ligament (PCL) in the knee's posterolateral stability and the magnitude of the coupled posterolateral instability with the knee examined at 90 degrees of flexion. The coupled posterolateral instability of the knee was studied by selective ligament cutting in cadaver knees set at 90 degrees. The coupled posterolateral displacement after cutting the PCL was 173% of the intact knee. With an intact PCL, the coupled posterolateral displacement after cutting the popliteus tendon and lateral collateral ligament with the knee at 90 degrees of flexion was 299% of the intact knee. When the PCL was cut together with the popliteus tendon and lateral collateral ligament, the coupled posterolateral displacement was 367%. The PCL plays an important role in the posterolateral stability of the knee, and its injury may cause mild (< 5 mm) to moderate (5-10 mm) posterolateral instability. Thus, in a knee with posterolateral instability, injury of the PCL must be considered. With an intact PCL, the posterolateral instability was very recognizable with the knee at 90 degrees of flexion, and injury to the PCL further increased the posterolateral instability and caused posterior translation of the knee. Therefore, examination for posterolateral instability of the knee should also be performed with the knee at 90 degrees of flexion, which is much easier to perform in a clinical setting. A positive posterior translation rather than posterolateral instability at different knee positions differentiates knees with combined PCL and posterolateral instability from knees with isolated posterolateral instability.

Cadaver↗
PubMed2004

Genomic heterogeneity and instability in colorectal cancer: spectral karyotyping, glutathione transferase-Ml and ras.

Genomic instability in cancer is frequently described as being either chromosomal instability or microsatellite instability, although when events within chromosomes are monitored, extensive intrachromosomal instability is also found. Spectral karyotyping was used to visualize how extensively genomic instability gives rise to intratumor genomic heterogeneity in sporadic colorectal carcinomas. Two factors were then examined which might relate to intrachromosomal instability in colorectal cancers: the presence of the glutathione transferase-Ml gene to detoxify potential carcinogens, and the presence of activated ras which has been associated with chromosomal instability when first expressed. Intrachromosomal genomic instability was previously determined by inter-(simple sequence repeat) PCR (inter-SSR PCR) and by fractional allelic loss rate for 348 markers. GSTM1 status was determined for each of 49 tumors through use of specific PCR, and 28 of the tumors showed the GSTM1 null genotype. A significant association was found between GSTMl-null status and elevated inter-(simple sequence repeat) PCR instability. In contrast, no association was found with fractional allelic loss rate. The first exons of the K-ras and H-ras oncogenes were sequenced in 72 colorectal cancers; 19 of the tumors had a mutation in codon 12 of the K-ras gene (24.5%), but no H-ras mutations were found. A weak correlation (p=0.10) was observed between mutant K-ras and inter-(simple sequence repeat) PCR genomic instability, and no association existed with fractional allelic loss rate.

Colorectal Neoplasms↗
PubMed2005

Pituitary tumour transforming gene (PTTG) induces genetic instability in thyroid cells.

Cancer reflects the progressive accumulation of genetic alterations and subsequent genetic instability of cells. Cytogenetic studies have demonstrated the importance of aneuploidy in differentiated thyroid cancer development. The pituitary tumour transforming gene (PTTG), also known as securin, is a mitotic checkpoint protein which inhibits sister chromatid separation during mitosis. PTTG is highly expressed in many cancers and overexpression of PTTG induces aneuploidy in vitro. Using fluorescent intersimple sequence repeat PCR (FISSR-PCR), we investigated the relationship between PTTG expression and the degree of genetic instability in normal and tumorous thyroid samples. The genomic instability index (GI index) was 6.7-72.7% higher in cancers than normal thyroid tissues. Follicular thyroid tumours exhibited greater genetic instability than papillary tumours (27.6% (n=9) versus 14.5% (n=10), P=0.03). We also demonstrated a strong relationship between PTTG expression and the degree of genetic instability in thyroid cancers (R2=0.80, P=0.007). To further investigate PTTG's role in genetic instability, we transfected FTC133 thyroid follicular cells and observed increased genetic instability in cells overexpressing PTTG compared with vector-only-transfected controls (n=3, GI Index VO=29.7+/-5.2 versus PTTG=63.7+/-6.4, P=0.013). Further, we observed a dose response in genetic instability and PTTG expression (GI Index low dose (0.5 microg DNA/ six-well plate) PTTG=15.3%+/-1.7 versus high dose (3 microg DNA) PTTG=50.8%+/-3.3, P=0.006). Overall, we describe the first use of FISSR-PCR in human cancers, and demonstrate that PTTG expression correlates with genetic instability in vivo, and induces genetic instability in vitro. We conclude that PTTG may be an important gene in the mutator phenotype development in thyroid cancer.

Caspase 3↗
PubMed2000

Retro-dental reactive lesions related to development of myelopathy in patients with atlantoaxial instability secondary to Os odontoideum.

STUDY DESIGN: A retrospective analysis of 13 patients with atlantoaxial instability secondary to Os odontoideum who underwent posterior atlantoaxial fusion. OBJECTIVE: To assess the relationships between the development of myelopathy and plain radiographic parameters in patients with atlantoaxial instability secondary to Os odontoideum and to determine whether the pathologic structures, which compress the spinal cord, are visualized using magnetic resonance imaging. SUMMARY OF BACKGROUND DATA: The development of myelopathy, which is the most serious complication associated with Os odontoideum, was thought to be related to either the degree of instability or direction of instability, or a decrease in the space available for the cord. However, such indirect radiographic parameters measured using plain radiographs cannot provide direct information concerning the causes of myelopathy in patients with atlantoaxial instability secondary to Os odontoideum. METHODS: Thirteen patients who underwent posterior atlantoaxial fusion for clinical symptoms due to Os odontoideum were classified into two groups depending on whether they had (n = 9) or did not have (n = 4) myelopathy. Four radiographic parameters were measured using flexion and extension lateral radiographs; the degree of instability, the direction of instability, and the space available for the cord in flexion and extension. MRI was performed on all patients in the myelopathy group. The radiologic and clinical data were compared for the two groups. RESULTS: There were no significant statistical differences in the degree of instability (6.83 vs. 7.38, P = 0.816), space available for the cord in flexion (6.94 vs. 7.13, P = 0.938), and space available for cord in extension (7.56 vs. 5.75, P = 0.434) between the two groups. There was a poor agreement between the direction of instability and the development of myelopathy (kappa = 0.268, P = 0.308). Magnetic resonance imaging did demonstrate, however, cord compression caused by retro-dental reactive lesions in the myelopathy; cystic masses were present in two patients; and fibrocartilaginous masses were present in seven. CONCLUSION: The current study suggests that the value of plain radiographic parameters should be reevaluated as a means of evaluating myelopathy in patients with atlantoaxial instability secondary to Os odontoideum, and that retro-dental reactive lesions should be considered as the potential cause of myelopathy.

Adult↗
PubMed2004

A soft tissue attempt to stabilize the multiply operated glenohumeral joint with multidirectional instability.

Treating patients with multidirectional instability who have had multiple failed stabilization procedures is a challenging problem. These patients have disability from instability and pain. Final treatment may be glenohumeral narthrodesis. We report on the results of a soft tissue operation for treatment of multidirectional instability in multiply operated shoulders. Since 1994, 28 patients have had what we term the kitchen sink operation for treatment of refractory multidirectional instability. After exclusion of patients with collagen abnormality, 10 patients who had at least three previous stabilizations were identified with recalcitrant multidirectional instability. The kitchen sink operation encompasses a humeral-based inferior capsular shift, Nicola biceps tenodesis, and coracohumeral ligament and rotator interval augmentation and/or reconstruction. All patients were immobilized for 8 weeks postoperatively. Minimum clinical and radiographic followup was 2 years (range, 2-6 years). Preoperatively, all patients had incapacitating pain and instability. Postoperatively, five patients (50%) had significant improvement of pain, and nine patients (90%) had successful reduction of instability. Four of the five patients with persistent disabling pain needed glenohumeral fusions. The kitchen sink operation is a final attempt to stabilize the shoulder with multidirectional instability. This procedure reduces instability (especially inferior) associated with multidirectional instability. However, pain remains unremitting in 50% of patients, therefore a glenohumeral arthrodesis may be needed as a last option.

Adult↗
PubMed2005

Wrist ligaments: their significance in carpal instability.

BACKGROUND: Understanding the exact contribution of the supporting ligaments to the functional integrity of the wrist is crucial for the diagnosis and treatment of carpal instabilities. The present study evaluates functional significance of the wrist ligaments with respect to carpal instabilities. MATERIALS AND METHODS: Sixteen fresh cadaver wrists were dissected. Extrinsic and intrinsic ligaments of the wrists (ligamentum radioscaphocapitatum, ligamentum radiolunotriquetrum and ligamentum triquetrohamatocapitatum) were sectioned sequentially. After sectioning of each ligament, the wrist was examined for clinical signs of instability such as misalignement of carpal bones, limited range of motion and dorsal translation. When instability was suspected, radiographs were taken and if instability was confirmed, then the ligament was repaired. RESULTS: Although none of the dorsal ligaments sectioning resulted in instability, sectioning of ligamentum scaphotrapeziotrapezoideum, ligamentum radioscaphocapitatum, ligamentum radiolunotriquetrum and ligamentum triquetrohamatocapitatum displayed scaphotrapeziotrapezoidal, dorsal intercalated segment, lunotriquetral and capitohamate instability respectively. In two wrists with arthrosis, sectioning of all ligaments didn't lead to any instability. CONCLUSION: Instability of the wrist can be classified on anatomical basis after the name of these four ligaments involved i.e. l. scaphotrapeziotrapezoideum, l. radioscaphocapitatum, l. radiolunotriquetrum and l. triquetrohamatocapitatum respectively . This approach clarifies the etiology and treatment of carpal instabilities.

Cadaver↗
PubMed1988

Postdecompression lumbar instability.

In the last two decades, the concept of spinal stenosis and its treatment by surgical decompression has been widely accepted. Complications such as olisthy, disc rupture, facet fracture, and intractable back pain began to appear postoperatively, suggesting instability as their cause. A retrospective study of 344 patients treated surgically for lumbar stenosis revealed a 17% reoperation rate for complications resulting from obvious or suspected instability. Sixteen cases of postdecompression olisthy, 14 cases of fresh disc herniation, and 27 cases of intractable back pain required further surgery. Preoperative indicators of potential instability are degenerated discs as evidenced by traction spurs or diminished disc height, olisthy, and scoliosis or asymmetrically narrowed discs. Total facetectomy and pars excision at surgery destabilize the spine and must be added to the preoperative risk factors for instability. Calcified annulus, capsule and ligamentum flavum, or complete disc resorption may offer some protection from postoperative instability. The level of instability may be preselected by the proximity to the intercrestal line. It is recommended that during surgical decompression for spinal stenosis, the posterior elements be spared as much as possible to avoid instability after surgery. Factors suggesting instability noted preoperatively or decompression which produces instability suggest that fusion should be combined with decompression. Spinal fusion is the treatment for postoperative instability.

Adult↗
PubMed1995

Management of multidirectional instability.

Since 1980, several authors have reported successful treatment of multidirectional instability with use of the inferior capsular shift. Neer's initial report in a series of 32 patients noted only one unsatisfactory result. One decade later he reported that ¿more than 100 additional inferior capsular shifts have been done with similar satisfactory results.¿ The authors have reported preliminary results following 75 inferior capsular shifts performed in young athletes. Eighty-nine percent were able to return to their major sport while seventy-three percent maintained the same level of competitiveness. Seven patients (9.3%) reported a single episode of probable subluxation that was not followed by recurrent instability and did not affect the final result, whereas two patients (2.7%) dislocated postoperatively. Both of these cases were associated with a traumatic episode. The average loss of external rotation was 7 deg. Altchek and Warren reported their results following a T-plasty modification of the Bankart procedure for multidirectional instability in 42 shoulders. The patient population differed somewhat because 38 of the 42 cases had a Bankart lesion or detachment of the labrum and glenohumeral ligament complex. Patient satisfaction was rated excellent for 40 (95%) of the shoulders. The average loss of external rotation was 5 deg. Altchek and Warren noted that throwing athletes were unable to throw a ball with as much speed as before the operation. Additionally, 7 of 42 shoulders (16%) demonstrated 2+ or greater posterior instability postoperatively. There were four cases of symptomatic recurrent instability, one anterior and three posterior, while one patient required a posterior stabilization 2 years postoperatively. Recently Cooper and Brems' reviewed their series of 43 shoulders in 38 patients with a minimum 2-year follow-up after inferior capsular shift. Thirty-nine of 43 shoulders (91%) were rated by the patient as satisfactory with no recurrent instability. Postoperatively recurrent symptomatic instability developed in four patients (11%). Two of these patients required subsequent revision inferior capsular shifts and one of those went on to a humeral head replacement for arthritis of dislocation. The latter patient had received a prior Bristow procedure. Cooper and Brems concluded that the inferior capsular shift procedure provided satisfactory objective and subjective results. Failures and recurrences of symptomatic instability generally occurred in the early postoperative period less than 2 years following surgery. Their findings did not demonstrate a deterioration of the results, with a follow-up of 6 years. The authors recently reported the results after inferior capsular shift from classic multidirectional instability in 52 shoulders. Thirty-six shoulders were approached from the anterior side and 16 from posterior. All were completely immobilized in a brace for 6 weeks postoperatively. Forty-nine shoulders were observed over 2 to 11 years (average: 5 years). Satisfactory results were achieved in 94% of cases. Turkel and coworkers demonstrated that anterior glenohumeral stability is provided by varying regions of the capsule depending on arm position. Similarly, Warner and coworkers have recently demonstrated that inferior humeral translation is restrained by the anterosuperior capsule and ligaments with the arm at the side, and by the inferior capsule and ligaments with the arm in abduction. This is consistent with the clinical findings of Neer and Foster, who described inferior humeral translation with the arm at the side and with the arm in abduction in patients with multidirectional instability, and emphasized reducing redundant capsular volume on all sides at the time of surgical reconstruction. The capsular shift procedure eliminates laxity in the rotator interval, anterosuperior capsule, and anteroinferior capsule.(ABSTRACT TRUNCATED)

Arm Injuries↗
PubMed1995

Microsatellite instability in human colonic cancer is not a useful clinical indicator of familial colorectal cancer.

BACKGROUND & AIMS: Microsatellite instability is a property of most tumors occurring in the context of hereditary nonpolyposis colon cancer. Instability also occurs in 10%-15% of apparently sporadic colorectal cancers, and it has been hypothesized that this instability may indicate a genetic predisposition to colonic cancer. This study evaluated whether there is a clinically useful association between colon cancer instability and a family history of cancer. METHODS: Colon cancer cases (n = 188) from a population-based study were evaluated for microsatellite instability with 10 polymerase chain reaction primer sets. Instability results were compared with family history and other clinical and biological characteristics. RESULTS: Microsatellite instability was found in 16.5% of tumors. It was predominantly a feature of right-sided tumors (P = 0.003) and was associated with the youngest and oldest ages at diagnosis (P = 0.01). Instability was not associated with family history of cancer, sex of the individual, or the glutathione-S-transferase mu 1 null genotype. CONCLUSIONS: Although some very small, and as yet undefined, proportion of colon cancer may be caused by inherited mutations leading to microsatellite instability, tumoral instability by itself is not a marker for familiality and should not be considered as evidence for an inherited syndrome.

Adult↗
PubMed1997

Genetic instability in colorectal cancers.

It has long been considered that genetic instability is an integral component of human neoplasia. In a small fraction of tumours, mismatch repair deficiency leads to a microsatellite instability at the nucleotide sequence level. In other tumours, an abnormal chromosome number (aneuploidy) has suggested an instability, but the nature and magnitude of the postulated instability is a matter of conjecture. We show here that colorectal tumours without microsatellite instability exhibit a striking defect in chromosome segregation, resulting in gains or losses in excess of 10(-2) per chromosome per generation. This form of chromosomal instability reflected a continuing cellular defect that persisted throughout the lifetime of the tumour cell and was not simply related to chromosome number. While microsatellite instability is a recessive trait, chromosomal instability appeared to be dominant. These data indicate that persistent genetic instability may be critical for the development of all colorectal cancers, and that such instability can arise through two distinct pathways.

Aneuploidy↗