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Results for “elevational migration”

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At least 595 records · Page 33Linked to original sources
PubMed2002

Elevated levels of circulating CD44 in patients with systemic sclerosis: association with a milder subset.

OBJECTIVE: To determine serum levels of soluble CD44 (sCD44), one of the adhesion molecules that regulate the migration of leucocytes, and clinical associations of these levels in patients with systemic sclerosis (SSc). METHODS: Serum sCD44 levels were examined by enzyme-linked immunosorbent assay. RESULTS: Serum sCD44 levels were elevated in SSc patients compared with normal controls. Serum sCD44 levels were higher in patients with limited cutaneous SSc than in those with diffuse cutaneous SSc. Patients with elevated sCD44 levels had pulmonary fibrosis less frequently than those with normal sCD44 levels. Serum sCD44 levels remained elevated during the follow-up in almost all patients with elevated levels at their first visit, whereas they remained normal in all patients with normal levels. CONCLUSION: Elevated sCD44 levels were associated with a relatively mild subset of SSc. These results suggest that CD44 could be a potential therapeutic target in SSc.

Adolescent↗
PubMed2003

Migratory costs and contemporary evolution of reproductive allocation in male chinook salmon.

Energetically demanding migrations may impact the resources available for reproductive trait development and activity, and hence favour evolution of new investment strategies for remaining resources. We conducted a large-scale experiment to evaluate the proximate cost of migration on male reproductive investment in chinook salmon (Oncorhynchus tshawytscha) and contemporary evolution of reproductive allocation. Experimentally induced differences in migratory costs (17 km inland and 17 m elevation vs. 100 km and 430 m) influenced dorsal hump size and upper jaw length, two traits influencing male mating success that are developed during migration. Longer migration also reduced tissue energy reserves available for competition and length of breeding life. Corresponding shifts in the balance between natural and sexual selection appear to have been responsible for heritable population divergence in secondary sexual trait investment, in approximately 26 generations, following colonization of spawning sites with different migratory demands.

Adaptation, Physiological↗
PubMed2002

Enhancement of reperfusion injury by elevation of microvascular pressures.

Elevated venous pressure can be associated with severe tissue injury. Few links, however, between venous hypertension and tissue damage have been established. We examined here the effects of micropressure elevation on the outcome of venular occlusion/reperfusion in the mesenteric microvasculature of male Wistar rats. One hour of venular occlusion (diameter approximately 50 microm) by micropipette occlusion followed by reperfusion were carried out with sham surgery without occlusion as control. Leukocyte rolling, adhesion, and migration, oxygen radicals detected by dichlorofluorescein (DCF), and parenchymal cell death detected by propidium iodide (PI) were recorded simultaneously in the same vessel at a location upstream of the occlusion site with elevated micropressure and at a downstream location with low micropressure. The number of rolling, adhering, and migrating leukocytes increased on the upstream side of the occlusion to a higher level than downstream of the occlusion site. During occlusion, DCF intensity on the venular endothelium was greater on the upstream side than in the downstream side, but there were no differences during reperfusion. The number of PI-positive cells adjacent to the venules increased significantly compared with controls, and it remained greater on the upstream higher-pressure side than the downstream side. Leukocyte adhesion and transvascular migration in postcapillary venules as well as parenchymal cell death could be significantly reduced by the hydroxyl radical scavenger dimethylthiourea. Microhemorrhages of blood cells into the mesentery interstitium were observed only on the upstream side of the occlusion. These results indicate that an elevation of the venular blood pressure during occlusion/reperfusion exacerbates the inflammatory cascade and tissue injury. Venous occlusion may constitute an important mechanism for tissue injury.

Animals↗
PubMed2006

IL-1beta stimulates rat cardiac fibroblast migration via MAP kinase pathways.

The pro-inflammatory cytokines interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) are elevated following acute myocardial infarction (MI) and have been implicated in the pathophysiology of cardiac disease progression. The cardiac fibroblast represents an important effector cell target for cytokine actions. In particular, cytokine-directed cardiac fibroblast migration is likely to impact both myocardial repair following acute MI and pathological myocardial remodeling in the progression to heart failure. In the present study, we examined the migratory response of neonatal rat cardiac fibroblasts to pro-inflammatory cytokines using modified Boyden chamber assays. On the basis of the knowledge of migration in other cell types, we hypothesized that members of the mitogen-activated protein kinase (MAPK) family may regulate this process. This possibility was addressed with the use of immunoblot detection of active phosphorylated MAPK species and pharmacological inhibitors for individual members of the MAPK cascades. IL-1beta stimulated robust and concentration-dependent increases in migration (maximum, 20-fold over control cells). TNF-alpha had lesser effect (fourfold increase over control). IL-6 did not induce migration. Activation of all three MAPK subfamilies (extracellular signal-regulated kinases, c-Jun NH(2)-terminal kinases, and p38) was shown to occur in response to cytokine stimulation. Fibroblast migration was attenuated by pharmacological inhibition of each MAPK subfamily. Understanding the regulation of cardiac fibroblast migration may provide insights in the search for therapies aimed at enhancing the functional nature of the remodeling process.

Animals↗
PubMed1998

Concentration-dependent stimulation of intestinal phase III of migrating motor complex by circulating serotonin in humans.

1. The influence of circulating 5-hydroxytryptamine (serotonin) on small intestinal motility was investigated in healthy volunteers. 2. Small intestinal motility was studied by means of a constantly perfused multi-channel manometry tube, connected to a computer system. 3. Intravenous infusions of either 5-hydroxytryptamine at increasing doses or saline were given over a period of 4 h. 4. 5-Hydroxytryptamine infusion dose-dependently increased plasma 5-hydroxytryptamine from approximately 2 to 10 and 25 nmol/l respectively, as well as urinary excretions of 5-hydroxytryptamine and 5-hydroxyindole acetic acid, a major 5-hydroxytryptamine metabolite. 5. The number of phase III of the migrating motor complex originating in the small intestine was dose-dependently increased by 5-hydroxytryptamine, and found to correlate to the plasma concentration of 5-hydroxytryptamine. The fraction of phase III also increased at the expense of phase II activity. In addition, 5-hydroxytryptamine increased the motility index, propagation velocity of phase III activity and the amplitude of contractions during phase III. 6. Whereas the low dose of 5-hydroxytryptamine (15 nmol.min-1.kg-1) had no haemodynamic effects, an increase in heart rate by approximately 20 beats/min, without change in blood pressure, was observed at the higher dose (60 nmol.min-1.kg-1). Respiratory parameters did not change during infusion of 5-hydroxytrytamine at either dose. 7. In conclusion, elevation of circulating 5-hydroxytryptamine by intravenous infusion results in more frequent and faster propagating migrating motor complexes in the human small intestine during the inter-digestive period.

Adult↗
PubMed1997

Macular holes: migratory gaps and vitreous as obstacles to glial closure.

PURPOSE: Retinal glia may play an important role in the closure of macular holes. This in vitro study examines whether and how the specific pathoanatomy, including foveal eversion and foveal vitreous, may interfere with glial closure of macular holes. METHODS: Culture dishes used to grow glial cells were modified by the placement of slopes, vertical steps, and gaps to mimic the in vivo migratory surface in and surrounding macular holes. In separate experiments, defects were made in a rodent glial monolayer. These defects were exposed to hyaluronic acid (HA) and to rabbit (RV) and bovine (BV) vitreous gel. The migratory behavior and completeness of closure of defects were compared to controls. RESULTS: As expected, glial cells migrated further and in greater numbers on a smooth surface. Slopes and steps were moderate obstacles to migration; gaps in the surface were absolute obstacles. HA modified the pattern of adhesion of cells at the bottom of defects. Defects in the glial monolayer were repaired in 5-7 days. Compared to these controls, repair was inhibited by 11% (n.s.), 28% (P = 0.02), and 58% (P = 0.004) after direct exposure of defects to HA, RV and BV, respectively. CONCLUSION: The elevated and everted margins of macular holes represent slope, step, and gap-like obstacles to the migration of glial cells and hence to the healing of defects. The defect allows extension of extracellular matrix into it and the subretinal space. Our results indicate that gaps in the migratory surface caused and aggravated by eversion and the presence of vitreous present obstacles to glial migration and closure of macular holes.

Animals↗
PubMedDate not supplied

Targeting of focal adhesion kinase by flavonoids and small-interfering RNAs reduces tumor cell migration ability.

Focal adhesion kinase (FAK), a member of a growing family of structurally distinct protein tyrosine kinases (PTK), has been linked to specific phosphorylation events, and the elevation of FAK activity in human carcinoma cells is associated with increased invasive potential. In the present study, therefore, we developed two experiments to test the hypothesis that FAK is a determinant of, and plays an important role in, regulating tumor cell migration. In the first, the biological functions of FAK were examined using flavonoid inhibition. MiaPaCa-2 cells, treated with luteolin (Lu) and quercetin (Qu), were used to dampen FAK phosphorylation and protein expression by parallel suppression of cell migration ability. The second experiment involved suppression of FAK expression using small-interfering RNAs (siRNA) specific to FAK. While not affecting cellular proliferation or apoptosis, the siRNA targeting FAK almost completely inhibited FAK protein expression in MiaPaCa-2 cells and potently blocked the cell migration mediated by FAK. Our results show that FAK functions as a key regulator of cell migration, and that FAK activity can be suppressed by specific FAK siRNA, and by luteolin and quercetin. It appears reasonable to conclude, therefore, that suppression of FAK protein has a significant impact on tumor cell invasiveness.

Cell Growth Processes↗
PubMed1978

[Leukocyte migration test and determination of carcinoembryonic antigens in the postoperative follow-up care of colon and rectum carcinoma].

Preoperative and serial postoperative CEA determinations have become widely accepted tools to aid the early detection of recurrent colorectal cancer. The panel modification of the direct leukocyte migration test (LMT) has proved to be an excellent monitor in these tumor patients. In this study LMT and CEA-RIA were compared. Peripheral blood leukocytes were pulsed with a high dose (2.5 and 0.5 mg/ml) of 3 m KCl extracts of five different colorectal tumors as well as with one 3m KCL extract of normal colonic mucosa. Patients showing a pathologic migration index (less than 0.80 and greater than 1.17) of 3 or more out of five tumor extracts were considered to be "positives." With this test mode 51 of 59 (86%) patients with resectable tumors were reactive, while only 24 of 69 (41%) yielded elevated CEA values. Both LMT and CEA-RIA were positive in 12 of the 13 patients with nonresectable tumors. After curative surgery most patients' leukocyte migration and CEA values were in tne normal range. Of the nine patients with localized tumor recurrence, eight were LMT reactive and five showed elevated CEA values. Of five patients with distant metastases, four demonstrated a positive reaction in the LMT and five a rise in CEA levels. The combination of the LMT with the CEA-RIA promises to improve the detection of recurrent colorectal cancer before the appearance of clinical evidence of recurrence.

Carcinoembryonic Antigen↗
PubMed2004

Homocysteine inhibits cardiac neural crest cell formation and morphogenesis in vivo.

Elevated homocysteine increases the risk of neurocristopathies. Here, we determined whether elevating homocysteine altered the proliferation or number of chick neural crest cells that form between the midotic and third somite in vivo. Homocysteine increased the number of neural tube cells but decreased neural crest cell number. However, the sum total of cells was not different from controls. In controls, the 5-bromo-2'-deoxyuridine-labeling index was higher in newly formed neural crest cells than in their progenitors, paralleling reports showing these progenitors must pass the restriction point before undergoing epithelial-mesenchymal transition. Homocysteine decreased the labeling index of newly formed neural crest cells, suggesting that it inhibited cell cycle progression of neural crest progenitors or the S-phase entry of newly formed neural crest cells. Homocysteine also inhibited neural crest dispersal and decreased the distance they migrated from the neural tube. These results show neural crest morphogenesis is directly altered by elevated homocysteine in vivo. Developmental Dynamics 229:63-73, 2004.

Animals↗
PubMed2001

A study on the density and distribution of uterine Natural Killer cells at mid pregnancy in mice genetically-ablated for CCR2, CCR 5 and the CCR5 receptor ligand, MIP-1 alpha.

Several chemoattractants mediate Natural Killer (NK) cell migration. The CC-chemokines, monocyte inflammatory protein (MIP)-1 alpha, regulated upon activation, normal T cell expressed and secreted (RANTES) and macrophage chemotactic protein (MCP)-1 are the most potent. Peripheral NK cells express the CC-chemokine receptor CCR2, for MCP-1 and CCR5, for MIP-1 alpha and RANTES. These chemokines are detected in the uterus during the estrous cycle and become elevated during pregnancy. To assess the roles of CCR2, CCR5 and MIP-1 alpha in NK cell migration to the uterus and localization within implantation sites, histological analysis was conducted on implantation sites from mice genetically-ablated for CCR2, CCR5, MIP-1 alpha or CCR2 and MIP-1 alpha. Uterine NK (uNK) cell densities in both the decidua basalis and mesometrial lymphoid aggregate of pregnancy (MLAp) of all mutant strains matched wildtype controls. Ratios of vascular: non-vascular uNK cell position were identical in mutants and controls. In the decidua basalis, 25-35% and in the MLAp, 15-20% of uNK cells were perivascular. Intravascular uNK cells were observed in the decidua basalis but not in the MLAp and were more numerous at gestation day 10 than 12. Two measures of uNK cell activation, cell diameter and cytoplasmic granule number, were similar in the mutants and controls. Thus, migration, distribution and activation of NK cells within the pregnant uterus are independent of CCR2, CCR5 and MIP-1 alpha.

Animals↗
PubMed2004

Cooperation of the ErbB2 receptor and transforming growth factor beta in induction of migration and invasion in mammary epithelial cells.

MCF10A mammary epithelial cells form growth-arrested structures when cultured in three-dimensional basement membrane gels. Activation of the receptor tyrosine kinase ErbB2 induces formation of proliferative structures that share properties with noninvasive early stage lesions. We conducted a genetic screen to identify cDNAs that can cooperate with ErbB2 to induce migration in these cells, with the hypothesis that they would represent candidate "second hits" in the development of invasive breast carcinomas. We found that expression of transforming growth factor (TGF)beta1 and TGFbeta3 in cells expressing activated ErbB2 induces migration in transwell chambers and invasive behavior in both basement membrane cultures and invasion chambers. The ability of ErbB2 to cooperate with TGFbeta correlated with sustained, elevated activation of extracellular signal-regulated kinase (Erk)-mitogen-activated protein kinase. Pharmacological reduction of Erk activity inhibited the cooperative effect of TGFbeta and ErbB2 on migration and expression of activated Erk kinase was sufficient to cooperate with TGFbeta to induce migration and invasion, suggesting that sustained Erk activation is critical for ErbB2/TGFbeta cooperation. In addition, we show that costimulation of ErbB2 and TGFbeta induces autocrine secretion of factors that are sufficient to induce migration, but not invasion, by means of both epidermal growth factor receptor-dependent and -independent processes. These results support the role of TGFbeta as a pro-invasion factor in the progression of breast cancers with activated ErbB2 and suggest that activation of the Erk and epidermal growth factor receptor pathways are key in mediating these events.

Breast Neoplasms↗
PubMed1997

Chemokine-enhanced migration of human peripheral blood mononuclear cells is antagonized by interferon beta-1b through an effect on matrix metalloproteinase-9.

The increased migration of peripheral blood mononuclear cells (PBMNCs) across a fibronectin (FN) matrix in response to the chemokines RANTES, MIP-1 alpha and MCP-1 is antagonized by interferon-beta-1b (IFN beta-1b). MCP-1 treatment of PBMNCs elevates their mRNA level and secretion of a matrix degrading enzyme, matrix metalloproteinase (MMP)-9, which is abrogated by IFN beta-1b. The clinical benefits of IFN beta-1b treatment in multiple sclerosis patients may in part be a result of this drug's ability to decrease the migration of PBMNCs in spite of a chemotactic gradient. Furthermore, the elevation of MMP-9 production by PBMNCs may be an important mechanism of action of chemokines.

Cell Migration Inhibition↗
PubMedDate not supplied

Fever of unknown origin caused by adult juvenile rheumatoid arthritis: the diagnostic significance of double quotidian fevers and elevated serum ferritin levels.

Fever of unknown origin (FUO) in adults is a commonly encountered clinical problem. Treatable causes of FUO in the adult should be the primary focus of the diagnostic workup. Neoplasms have replaced infectious diseases as being the most common cause of FUO in adults, and collagen vascular diseases are now relatively rare. The most important collagen vascular diseases presenting as an FUO include Takayasu's arteritis, Kikuchi's disease, polymyalgia rheumatica, and adult juvenile rheumatoid arthritis (JRA) (adult Still's disease). There are no specific diagnostic tests for these disorders, which commonly present as prolonged fevers that are not easily diagnosed (i.e., FUO). Adult JRA is a rare but important cause of FUO in adults. Typically, patients with adult Still's disease present with liver/spleen involvement, posi-articular arthritis, ocular involvement, and evanescent salmon-colored truncal rash. An important diagnostic finding in adult JRA is the presence of a double quotidian fever, which occurs in few other disorders. Only visceral leishmaniasis and adult JRA are causes of FUO in adults associated with double quotidian fevers. Highly elevated serum ferritin levels are the most important nonspecific diagnostic finding associated with adult JRA. We present a case of FUO caused by adult JRA presenting with diffuse polyarticular migrating arthritis, evanescent rash, and splenomegaly. The diagnosis of adult JRA was suggested by these findings in association with a double quotidian fever and a highly elevated serum ferritin level. Clinicians should appreciate the diagnostic significance of fever patterns and the diagnostic significance of elevated serum ferritin levels in patients with FUO.

Adult↗
PubMed2004

LR11, an LDL receptor gene family member, is a novel regulator of smooth muscle cell migration.

LR11, a member of the LDL receptor family, is highly expressed in vascular smooth muscle cells (SMCs) of the hyperplastic intima, and induces enhanced migration of SMCs in vitro via its upregulation of urokinase-type plasminogen activator receptor (uPAR) expression. In this study, we have delineated the mechanism by which LR11 elevates the expression levels of uPAR in SMCs. Secretion of soluble LR11 is induced in SMCs during the rapidly proliferating phase, and the secreted LR11 induces the migration activities of SMCs. Both the cell-anchored and secreted forms of LR11 have the capacity to bind to and form complexes with uPAR. LR11-overexpressing cells show significantly enhanced uPAR binding, but decreased uPAR internalization. LR11 colocalizes with uPAR on the cell surface and inhibits the LDL receptor-related protein (LRP)-mediated binding and internalization of uPAR. Thus, LR11 mediates the uPAR localization to the plasma membrane. LR11 is highly expressed in the atheromatous plaque areas of apoE knockout mice, particularly in the intimal SMCs at the border between intima and media. The neutralization of LR11 function with anti-LR11 antibody reduced cuff-induced intimal thickness in mice. The novel mechanism of regulation of uPAR localization in SMCs accompanied with enhanced migration activity possibly constitutes an important factor in the process of atherosclerosis and arterial remodeling.

Animals↗
PubMed2001

Leptin stimulates rat aortic smooth muscle cell proliferation and migration.

Leptin, a peptide secreted from adipose tissue, plays an important role in the regulation of food intake and energy expenditure. In obese patients, plasma leptin levels are elevated and obesity is one of the major risk factors for cardiovascular diseases. Therefore, in this study, we investigated the effect of leptin on vascular smooth muscle cell (VSMC) functions. Cultured rat aortic VSMC expressed 130-kDa short form of leptin receptor. Leptin stimulated both proliferation and migration of VSMC. Leptin stimulated phosphorylation and activation of mitogen-activated protein (MAP) kinases, and also increased phosphatidylinositol (PI) 3-kinase activity. Further, two distinct PI 3-kinase inhibitors, wortmannin and LY294002 inhibited the migratory effect of leptin. These results demonstrate that leptin is a proliferative and migratory factor for VSMC, implying that leptin may play a role in the formation and development of vascular lesions.

Androstadienes↗
PubMed1997

Urokinase but not tissue plasminogen activator mediates arterial neointima formation in mice.

To define the role of the plasminogen activators (PAs) tissue PA (t-PA) and urokinase PA (u-PA) in vascular wound healing, neointima formation and reendothelialization were evaluated after electric or mechanical arterial injury in mice with a single or combined deficiency of t-PA (t-PA-/-) and/or u-PA (u-PA-/-). In both models, neointima formation and neointimal cell accumulation were reduced in u-PA-/- and in t-PA-/-/u-PA-/- arteries but not in t-PA-/- arteries. The electric injury model was used to characterize the underlying cellular mechanisms. Topographic analysis of vascular wound healing in electrically injured wild-type and t-PA-/- arteries revealed a similar degree of migration of smooth muscle cells from the noninjured borders into the necrotic center. In contrast, in u-PA-/- and t-PA-/-/u-PA-/- arteries, smooth muscle cells accumulated at the uninjured borders but failed to migrate into the necrotic center. Cultured u-PA-/- but not t-PA-/- smooth muscle cells also failed to migrate in vitro after scrape wounding. Proliferation of smooth muscle cells was not affected by PA deficiency. Reendothelialization after electric injury was similar in all genotypes. In situ analysis revealed markedly elevated u-PA zymographic activity, mRNA, and immunoreactivity in smooth muscle cells, endothelial cells, and leukocytes within 1 week after injury, eg, when cells migrated into the wound. Thus, u-PA plays a significant role in vascular wound healing and arterial neointima formation after injury, most likely by affecting cellular migration.

Animals↗
PubMed2024

Exploring the clinical and biological significance of the cell cycle-related gene CHMP4C in prostate cancer.

BACKGROUND: Prostate cancer (PCa) stands as the second most prevalent malignancy impacting male health, and the disease's evolutionary course presents formidable challenges in the context of patient treatment and prognostic management. Charged multivesicular body protein 4 C (CHMP4C) participates in the development of several cancers by regulating cell cycle functions. However, the role of CHMP4C in prostate cancer remains unclear. METHODS: In terms of bioinformatics, multiple PCa datasets were employed to scrutinize the expression of CHMP4C. Survival analysis coupled with a nomogram approach was employed to probe into the prognostic significance of CHMP4C. Gene set enrichment analysis (GSEA) was conducted to interrogate the functional implications of CHMP4C. In terms of cellular experimentation, the verification of RNA and protein expression levels was executed through the utilization of qRT-PCR and Western blotting. Upon the establishment of a cell line featuring stable CHMP4C knockdown, a battery of assays, including Cell Counting Kit-8 (CCK-8), wound healing, Transwell, and flow cytometry, were employed to discern the impact of CHMP4C on the proliferation, migration, invasion, and cell cycle function of PCa cells. RESULTS: The expression of CHMP4C exhibited upregulation in both PCa cells and tissues, and patients demonstrating elevated CHMP4C expression levels experienced a notably inferior prognosis. The nomogram, constructed using CHMP4C along with clinicopathological features, demonstrated a commendable capacity for prognostic prediction. CHMP4C knockdown significantly inhibited the proliferation, migration, and invasion of PCa cells (LNcaP and PC3). CHMP4C could impact the advancement of the PCa cell cycle, and its expression might be regulated by berberine. Divergent CHMP4C expression among PCa patients could induce alterations in immune cell infiltration and gene mutation frequency. CONCLUSIONS: Our findings suggest that CHMP4C might be a prognostic biomarker in PCa, potentially offering novel perspectives for the advancement of precision therapy for PCa.

Humans↗
PubMedDate not supplied

Arthroscopic subscapularis tendon repair: Technique and preliminary results.

PURPOSE: Our objective was to evaluate the preliminary results of 25 consecutive arthroscopic subscapularis tendon repairs. TYPE OF STUDY: Case series. METHODS: All 25 shoulders had longer than 3 months follow-up, with an average of 10.7 months (range, 3 to 48 months). The average age was 60.7 years (range, 41 to 78 years). The average time from onset of symptoms to surgery was 18.9 months (range, 1 to 72 months). The shoulders were evaluated using a modified UCLA score, Napoleon test, lift-off test, radiographs, and magnetic resonance imaging (MRI). Indications for surgery included clinical and/or MRI evidence of a rotator cuff tear. An arthroscopic suture anchor technique devised by the senior author (S.S.B.) was used for repair. RESULTS: UCLA scores increased from a preoperative average of 10.7 to a postoperative average of 30.5 (P <.0001). By UCLA criteria, excellent and good results were obtained in 92% of patients, with 1 fair and 1 poor result. Forward flexion increased from an average 96.3 degrees preoperatively to an average 146.1 degrees postoperatively (P =.0016). Eight of 9 patients with a positive Napoleon test had complete tears of the subscapularis. All 7 patients with a negative Napoleon test had a tear of the upper half only. The lift-off test could not be performed reliably due to pain or restricted motion in 19 of the 25 patients. Eight patients had isolated tears of the subscapularis. The remaining 17 patients had associated rotator cuff tears with an average total tear size of 5 x 8 cm. Ten patients had proximal migration of the humerus preoperatively. Eight of these 10 patients had durable reversal of proximal humeral migration following surgery. These 8 patients improved their overhead function from a preoperative "shoulder shrug" with attempted elevation of the arm to functional overhead use of the arm postoperatively. CONCLUSIONS: (1) The senior author has been able to consistently perform arthroscopic repair of torn subscapularis tendons, with good and excellent results, in 92% of patients. (2) The Napoleon test is useful in predicting not only the presence of a subscapularis tear, but also its general size. (3) Combined tears of the subscapularis, supraspinatus, and infraspinatus tendons are frequently associated with proximal humeral migration and loss of overhead function. Arthroscopic repair of these massive tears can produce durable reversal of proximal humeral migration and restoration of overhead function.

Adult↗