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PubMed2004

The role of meniscal root pathology and radial meniscal tear in medial meniscal extrusion.

OBJECTIVE: The purpose of our study was twofold: to better understand the relationship between medial meniscal extrusion (MME) and degenerative joint disease (DJD), and to determine whether a relationship exists between MME and medial meniscal root (MMR) pathology, radial tear and joint effusion. DESIGN AND PATIENTS: Two hundred and five consecutive MR imaging examinations of the knee were prospectively evaluated, regardless of indication, for the presence and degree of MME, medial compartment marginal osteophytes, medial compartment articular cartilage loss, joint effusion, medial meniscal tear and MMR pathology. MME >or=3 mm was considered abnormal. All studies were performed using a 1.5 T GE Signa MR unit with a quadrature knee coil. The standard protocol included oblique sagittal, coronal and axial imaging. RESULTS: We found a strong association ( P<0.0001) between >or=3 mm MME and medial joint line osteophytosis (77%), medial compartment articular cartilage loss (69%), MMR pathology (64%) and radial tear (58%) when compared with knees without these findings. Fifty-one percent of cases with a moderate/large joint effusion had <3 mm MME. We found that 20% (31/155) of patients with minimal or no evidence of DJD had >or=3 mm MME. Of this group, 62% (19/31) had either MMR pathology and/or radial tear, 13% (4/31) had joint effusion as their only abnormality and 6% (2/31) had a normal examination (other than the presence of MME). The remaining 19% consisted of three cases of different types of meniscal tear and three cases of small joint effusions but no other detectable pathology. CONCLUSION: MME >or=3 mm is strongly associated with DJD, MMR pathology and radial tear. A significant number of cases with no or minimal evidence of DJD (20%) had >or=3 mm MME, suggesting that MME precedes, rather than follows, the development of DJD. We also found that joint effusion was not strongly associated with >or=3 mm MME.

Adolescent↗
PubMed1997

Metalloelastase expression in a mouse macrophage cell line--regulation by 4beta-phorbol 12-myristate 13-acetate, lipopolysaccharide and dexamethasone.

The regulation of the expression of mouse macrophage elastase (MME) was investigated using the murine tumor cell line P388D1. The effects of three factors were studied: a phorbol ester (4beta-phorbol 12-myristate 13-acetate, PMA), an endotoxin (lipopolysaccharide, LPS) and a corticosteroid (dexamethasone). Both in situ hybridization and northern blot analysis showed that P388D1 cells constitutively express the MME gene. Quantification of the MME mRNA by northern blot analysis showed that only PMA and dexamethasone significantly regulate MME gene expression in a time-dependent and dose-dependent manner. After PMA treatment, the MME mRNA level was maximal between 4 h and 9 h (medium-term response), and the mean amplitude of the response to a concentration of 100 nM was 2.5-fold (P<0.01). LPS did not induce any significant change in MME mRNA level even when 1% serum was added to the cultures. Following dexamethasone treatment, the MME mRNA level was minimal between 21 h and 33 h (long-term response), and the mean amplitude of the response to a concentration of 100 nM was 0.49-fold (P < 0.05). Using actinomycin D, it appeared that the inhibition of RNA synthesis reduces the ulterior stimulating effect of PMA from 184% to 121%, and that MME mRNA has a half-life longer than 8 h, which is not diminished by dexamethasone. These results strongly suggest that the two factors modify MME mRNA level by stimulating (PMA) or inhibiting (dexamethasone) the transcription of the gene, rather than by modifying the transcript stability. Analysis of the cell-conditioned media by elastin zymography showed the MME as a lysis band in the 22-kDa region, the intensity of which varied with the treatments. The MME secretion is stimulated by PMA, inhibited by dexamethasone and does not show any variation after LPS treatment.

Animals↗
PubMed1999

Induction and regulation of macrophage metalloelastase by hyaluronan fragments in mouse macrophages.

Although the metalloproteinase murine metalloelastase (MME) has been implicated in lung disorders such as emphysema and pulmonary fibrosis, the mechanisms regulating MME expression are unclear. Low m.w. fragments of the extracellular matrix component hyaluronan (HA) that accumulate at sites of lung inflammation are capable of inducing inflammatory gene expression in macrophages (Mphi). The purpose of this study was to examine the effect of HA fragments on the expression of MME in alveolar Mphi. The mouse alveolar Mphi cell line MH-S was stimulated with HA fragments over time, total RNA was isolated, and Northern blot analysis was performed. HA fragments induced MME mRNA in a time-dependent fashion, with maximal levels at 6 h. HA fragments also induced MME protein expression as well as enzyme activity. The induction of MME gene expression was specific for low m.w. HA fragments and dependent upon new protein synthesis; it occurred at the level of gene transcription. We also examined the effect of HA fragments on MME expression in inflammatory alveolar Mphi from bleomycin-injured rat lungs. Although normal rat alveolar Mphi did not express MME mRNA in response to HA fragments, alveolar Mphi from the bleomycin-treated rats responded to HA fragment stimulation by increasing MME mRNA levels. Furthermore, baseline and HA fragment-induced MME gene expression in alveolar Mphi from bleomycin-treated rats was inhibited by IFN-gamma. These data suggest that HA fragments may be an important mechanism for the expression of MME by Mphi in inflammatory lung disorders.

Animals↗
PubMed2001

Mouse macrophage metalloelastase gene delivery by HVJ-cationic liposomes in experimental antiangiogenic gene therapy for murine CT-26 colon cancer.

We previously demonstrated that gene replacement of mouse macrophage metalloelastase (MME) into murine melanoma cells that grow rapidly and are MME deficient suppresses the primary tumor growth in vivo by halting angiogenesis. The aim of the present study was to evaluate the effectiveness of gene therapy against cancer using a cDNA-encoding MME gene. In a subcutaneous tumor model of CT-26 mouse colon cancer cells that are MME deficient, syngeneic mice repetitively treated with direct injections into the tumors of MME- hemagglutinating virus of Japan (HVJ), a type of HVJ-cationic liposome encapsulating a plasmid expressing MME, developed smaller tumors (210 +/- 47.2 mm(3) versus 925 +/- 156 mm(3) mean +/- SEM; p = 0.0004) with fewer microvessels (10.25 +/- 1.03 vs. 17.25 +/- 2.14; p = 0.03) than control mice. TUNEL staining revealed a significant increase of apoptotic cells in the MME-HVJ liposomes-treated tumors compared with control tumors. MME was effectively expressed in the s.c. tumors treated with MME-HVJ liposomes, inducing angiostatin generation in those tumors, as demonstrated by Western blot analysis. In conclusion, our study demonstrated that repeated in vivo transduction of the MME gene directly into the tumors using HVJ-cationic liposomes suppressed the tumor growth by an antiangiogenic mechanism, providing, then, a feasible strategy for gene therapy of cancer.

Angiostatins↗
PubMed2000

Mouse macrophage metalloelastase gene transfer into a murine melanoma suppresses primary tumor growth by halting angiogenesis.

Mouse macrophage metalloelastase (MME) has been associated with the generation of angiostatin, an internal fragment of plasminogen, which inhibits angiogenesis. To clarify whether tumor cells that consistently generate MME can suppress angiogenesis and, therefore, inhibit the growth of primary tumors in vivo, we transfected a cDNA coding for MME into murine B16-BL6 melanoma cells that grow rapidly and are MME deficient. The generation of active MME in MME-transfected clones was confirmed by immunoprecipitation followed by in vitro cleavage of plasminogen. Subcutaneous implantation of these stable clones in C57BL/6 mice inhibited primary tumor growth by an average of 73% (P = 0.00002), which directly correlated with a significant reduction of blood vessel formation (approximately 76%) in such tumors. Microangiography revealed massive angiogenesis in control tumors (mock and vector); however, in MME-transfected primary tumors it demonstrated a decreased and disrupted vascular network. Western blot analysis using a specific anti-mouse angiostatin antibody demonstrated a strong 38-kDa immunoreactive band in MME-transfected tumors and in the serum of mice bearing those tumor cells. These results show that placing MME gene directly into B16-BL6 melanoma cells is an effective approach to suppress primary tumor growth in vivo because it halts angiogenesis. Our data provide a feasible and promising strategy for gene therapy of cancer by targeting tumor vasculature.

Angiostatins↗
PubMed1992

Molecular cloning, chromosomal localization, and bacterial expression of a murine macrophage metalloelastase.

Murine macrophages have previously been shown to secrete a zinc-dependent proteinase that can degrade elastin. In this report, we identify murine macrophage elastase (MME) cDNA and show that it is a distinct member of the metalloproteinase gene family. Small amounts of MME were purified to homogeneity, and N-terminal amino acid sequence was obtained. This sequence was used to obtain a partial cDNA clone by the polymerase chain reaction; a cDNA library derived from a mouse macrophage-like cell line (P388D1) was screened with this probe. A full-length MME cDNA spanning approximately 1.8 kilobases contained an open reading frame of 1386 base pairs; the predicted molecular mass of the MME proenzyme is 53 kDa. The gene encoding MME is represented only once in the mouse genome and is located on chromosome 9. Despite a size that is similar to other metalloproteinases, MME is distinct, sharing only 33-48% amino acid homology with other metalloproteinases. In contrast to other metalloenzymes, MME appears to be rapidly processed to an active truncated form (N-terminal and C-terminal cleavage). We expressed recombinant MME in Escherichia coli and demonstrated that it has significant elastolytic activity that is specifically inhibited by the tissue inhibitor of metalloproteinases. MME is therefore a true metalloproteinase that may be involved in tissue injury and remodeling.

Amino Acid Sequence↗
PubMed1996

Monomethylethanolamine reduces plasma triacylglycerols and apolipoprotein B and increases apolipoprotein A-I rats without induction of fatty liver.

Monomethylethanolamine (MME) inhibits very low density lipoprotein (VLDL) secretion from cultured rat hepatocytes by disruption of translocation of apolipoprotein (apo) B across the endoplasmic reticulum membrane (A. E. Rusiñol, E. Y. W. Chan and J. E. Vance. 1993. J. Biol. Chem. 268: 25168-25175). We have now investigated whether or not plasma levels of lipids and apoB are reduced by dietary supplementation of rats with MME. In rats fed MME for 5 to 7 days, the levels of triacylglycerols and apoB in VLDL were reduced by 66% and 45%, respectively. At the same time, MME feeding also increased plasma apoA-I by 80%. No significant differences were found in body or liver weights between control and MME-fed rats, nor did the reduction of plasma VLDL in MME-fed rats result in accumulation of triacylglycerols in the liver. When the dietary period was extended to 15 weeks, essentially the same results were obtained except that plasma cholesterol was increased by 31% in MME-treated animals, apparently because of increased amounts of apoA-I and high density lipoproteins. According to post-mortem and microscopic examination, rats fed MME for 15 weeks were anatomically normal with no indication of any lipid accumulation in the liver. The ability of MME to reduce VLDL secretion and at the same time to increase the level of high density lipoproteins are attractive properties of a therapeutic agent for treatment of atherosclerosis in humans.

Animals↗
PubMed1999

Induction of metalloelastase mRNA in murine peritoneal macrophages by diethylmaleate.

Macrophage-specific metalloelastase (MME) hydrolyzes elastin and other matrix proteins and plays an important physiological role in tissue remodeling and pathological tissue destruction. We have examined the effects of diethylmaleate (DEM), an electrophilic agent that reacts with sulfhydryls, on the expression of MME mRNA in mouse peritoneal macrophages. Quantification of MME mRNA by Northern blot analysis revealed that basal mRNA levels were quite low in freshly isolated cells, although mRNA levels increased markedly and reached a steady level within 12 h when cells were cultured in a serum-supplemented RPMI 1640 medium. When macrophages were challenged with DEM at 0.05-1.0 mM for 8 h the expression of the MME gene was enhanced further. In the presence of 0.1 mM DEM, the level of the MME mRNA increased 2-fold compared to the control levels after 6-9 h and decreased to control levels in 24 h. Other electrophilic agents, catechol and 1-chloro-2,4-dinitrobenzene, also enhanced MME gene expression. However, oxidative stress agents such as hydrogen peroxide, menadione, paraquat (an O-2 generator), sodium arsenite and cadmium chloride had no effect on MME gene expression. These results indicate that the electrophilic agents selectively enhance the expression of MME mRNA during primary culture of the macrophages.

Animals↗
PubMed1996

Myoepithelial tumors of salivary glands: a clinicopathologic, immunohistochemical, ultrastructural, and flow-cytometric study.

Myoepitheliomas of the salivary glands remain a controversial entity. To contribute to the knowledge of this entity, 16 myoepithelial tumors of the salivary glands were studied: 12 benign myoepitheliomas (BME) and 4 malignant myoepitheliomas (MME). The clinical and the histologic findings of each case were studied Immunohistochemistry and flow-cytometry analysis were performed from the paraffin-embedded material in 15 cases. An electron-microscopy study was performed in 8 cases. The myoepithelial tumors affected patients of both sexes equally. The mean age of the patients with BME was 54 years, and the mean age of patients with MME was 62 years. Eight cases of BME originated in the parotid gland and 4 cases originated in the minor salivary glands. All the MME developed from a benign preexistent tumor: two developed from a pleomorphic adenoma in the parotid gland, and the other two MME developed in the minor salivary gland from a BME. The myoepithelial tumors were composed of epithelioid, plasmacytoid, spindle, or clear cell types, and they showed a solid or a myxoid pattern of growth. Immunohistochemical studies revealed marked and diffuse positivity to cytokeratins, vimentin, and S-100 protein in all cases. Glial fibrillary acidic protein was positive in 8 cases (53%), and muscle-specific actin and smooth-muscle actin were positive in only 3 cases (20%); they were all cases of BME. Desmin was negative in all tumors. Ultrastructural studies showed the presence of basal membrane, tight junctions, intermediate filaments, and microvilli as well as actin-like filaments lacking focal densities in all cases. But actin-like filaments with focal densities were not identified. Flow cytometry determined that all BME were diploid with a mean proliferative index of 7.73%. Two of the MME were diploid and the other two MME were aneuploid. The mean proliferative index of MME was 11.93%. In conclusion, BME and MME originated in major and minor salivary glands can display different histologic patterns and cellular features. Some immunohistochemical and ultrastructural characteristics have been found in all these neoplasms, which supports the idea that myoepitheliomas are composed by neoplastic modified myoepithelial cells, not fully differentiated. These techniques can be useful for the diagnosis of these tumors.

Adult↗
PubMed2000

Interleukin-2 induces cell cycle perturbations leading to cell growth inhibition and death in malignant mesothelioma cells in vitro.

Previous report indicated that Interleukin-2 (IL-2) is able to inhibit the growth of IL-2-receptor-positive cancer cell lines without any involvement of the immune system, through IL-2-induced alterations of the cell cycle kinetics. In this study we provide evidence that IL-2 exerts anti-proliferative effect on three human malignant mesothelioma (MMe) cells in vitro, while no effects were observed on normal human mesothelial cell (HMC) primary cultures. The growth inhibitory effect of IL-2 on neoplastic cells appeared to depend on the baseline proliferative status of these cells. Indeed, in highly proliferating MMe cells, we observed a reduction of malignant cells in the S-phase of the cell cycle, with an accumulation in G0/G1, followed by apotosis for longer incubations or exposure to higher doses. On the contrary, in MMe cells proliferating at lower rate, IL-2 induces only a late cytotoxic effect, leading to apoptosis, without significantly affecting the cell cycle. IL-2Rbeta mRNA was detectable by RT-PCR in all MMe cells, IL-2Ralpha mRNA in one only out the three assayed and IL-2Rgamma mRNA in none. In addition, mRNA specific for the IL-2Rbeta-associated Jak-1 tyrosine kinase was expressed in all MMe cell lines, further suggesting that IL-2Rbeta may play a role in the observed effects. Very low, albeit detectable, levels of IL-2Rbeta chain appeared to be expressed at the cell surface of MMe cells by indirect immunofluorescence and FACS analyses. Finally, Ca(++) fluxes were rapidly induced when MMe cells were exposed to exogenous IL-2.

Apoptosis↗
PubMed2006

Transfection of mouse macrophage metalloelastase gene into murine CT-26 colon cancer cells suppresses orthotopic tumor growth, angiogenesis and vascular endothelial growth factor expression.

A cDNA fragment coding for domains I and II of mouse macrophage metalloelastase (MME) was transfected into murine CT-26 colon cancer cells that are MME deficient. An orthotopic implantation model was established by using MME-transfected cells. In MME-transfected primary tumors, it demonstrated that tumor growth and microvessel formation were significantly inhibited compared with the controls. The expression of vascular endothelial growth factor (VEGF) mRNA and protein was significantly lower in MME-transfected group compared with those in the controls. Our data show that both MME and VEGF gene expression is highly associated with the vascularity of tumors, which may depend on a balance between MME and VEGF expression.

Animals↗
PubMed2002

Acute cigarette smoke-induced connective tissue breakdown requires both neutrophils and macrophage metalloelastase in mice.

The cells/proteases responsible for the development of smoke-induced emphysema is an area of intense investigation. Mice with knockout of macrophage metalloelastase genes (MME(-/-)) do not develop emphysema after smoke exposure, but we also observed that neutrophils (PMN) in lavage appeared to be a requirement for acute connective tissue breakdown. In this study we exposed mice to cigarette smoke and examined lavage PMN, macrophages (MAC), desmosine (DES, a measure of elastin breakdown) and hydroxyproline (HP, a measure of collagen breakdown) 24 h afterwards. MME(+/+) mice exposed to smoke showed elevations in PMN, DES, and HP, but no elevations were seen in MME-deficient mice. Both PMN influx and increased levels of DES/HP could be restored by administering MAC from MME(+/+) mice to MME-deficient mice and then exposing them to smoke. RS113456, a metalloprotease inhibitor, also prevented PMN influx and connective tissue breakdown. Western blots against mouse alpha(1)-antitrypsin (alpha(1)AT) showed that alpha(1)AT was not protected in MME-deficient mice, nor by administration of RS113456. We conclude that, in mice, acute smoke-induced connective tissue breakdown, the precursor to emphysema, requires both PMN and MME, that PMN influx appears to be secondary to MAC activation, and that this process initially does not involve protection of alpha(1)AT from metalloprotease attack.

Animals↗
PubMed1982

Mitral valve prolapse. Cross sectional and provocative M-mode echocardiography.

False-negative supine M-mode echocardiograms occur in some patients with proved mitral valve prolapse. To investigate further, we performed M-mode echocardiography (MME) during standing and after the inhalation of amyl nitrite in 17 patients (group 1) selected for auscultatory evidence of mitral valve prolapse (MVP) but negative supine MME. To validate the standing MME technique, eight patients with classic auscultatory MVP with positive supine MME for MVP (group 2) and 15 control subjects (group 3) were studied. Supine cross-sectional echocardiography (CSE) was compared to MME in all three groups. Standing MME elicited echocardiographic evidence of MVP in 14/17 (82 percent) of group 1--auscultatory evidence of MVP but negative supine MME; CSE demonstrated MVP in 8/13 (62 per cent) of the same patients. There was no clear advantage of the CSE long axis view over the CSE apical four chamber view in the diagnosis of MVP in these selected subjects; however, the two views were complementary. Amyl nitrite was ineffective in eliciting echocardiographic evidence of MVP.

Adult↗
PubMed2003

Transforming growth factor-beta released by PPD-presenting malignant mesothelioma cells inhibits interferon-gamma synthesis by an anti-PPD CD4+ T-cell clone.

Besides acting complexly on both normal and tumor cells, transforming growth factor-beta (TGF-beta) can determine the nature of the response to the antigen, strongly inhibiting the differentiation of naive CD4+ T-cells toward a T helper-1 (Th-1) phenotype; in a number of experimental models, TGF-beta also appeared to be a potent immunosuppressant factor. TGF-beta was shown to be released by some human malignant mesothelioma (MMe) cells, which affects the immune response to this tumor. Thus, for a better understanding of the role of TGF-beta in the immune response to MMe cells, we evaluated the production of a Th-1 cytokine (IFN-gamma) and of a Th-2 cytokine (IL-4), following Purified Protein Derivative (PPD) recall antigen presentation by human MMe cells to a class-II major histocompatibility complex (MHC-II)-matched PPD clone (PPD clone). Our data confirm that human MMe cells possess the unusual capability of presenting a common recall antigen to CD4+ lymphocytes but also show that these tumor cells can abrogate Th-1 immune response, as evidenced by a shift in favor of the production of IL-4 over that of IFN-gamma, through a TGF-beta-mediated pathway; only the simultaneous block of TGF-beta1 and beta2 effects can significantly restore a typical Th-1 pattern of cytokine production by PPD clone in response to PPD presentation by MMe. Even though the role of TGF-beta in the promotion of MMe growth should be further and better defined, this effect should be considered when designing new therapeutical approaches aimed at improving the immune response to MMe.

CD4-Positive T-Lymphocytes↗
PubMedDate not supplied

Malignant mesothelioma in 2004: How advanced technology and new drugs are changing the perspectives of mesothelioma patients. Highlights from the VIIth Meeting of the International Mesothelioma Interest Group.

Malignant mesothelioma (MMe) is a seemingly uncommon tumour whose incidence has in fact increased steadily and progressively over the last 30 years. Indeed, an actual "epidemic" is expected in the next 20 years, with over 1300 new cases a year till 2020 at least. Despite unquestionable improvement in the diagnostic methods at our disposal and the availability of new treatment strategies, the prognosis of MMe patients remains dramatically poor. For all the above reasons, translational research is the key to success; indeed, ever increasing knowledge of the molecular mechanisms underlying MMe pathogenesis could lead (and is actually leading) to new, hopefully more active, treatment options. To foster discussion among investigators working in this field, and to exchange different viewpoints concerning the newest advances in MMe pathogenesis and treatment, the VII International Mesothelioma Interest Group (IMIG) meeting was held in Brescia (Italy) between 24 and 26 June 2004 in cooperation with the Italian Group for the Study and Therapy of MMe (GIMe). The aim of this report is to summarize the most significant advances in the different disciplines applied to MMe presented and discussed during the IMIG meeting and how these advances will be changing the perspective of patients with MMe.

Angiogenesis Inhibitors↗
PubMed2006

Medial collateral ligament healing in macrophage metalloelastase (MMP-12)-deficient mice.

Medial collateral ligament (MCL) injuries heal by a wound repair scar response controlled by a complex cellular and cytokine environment. Many enzymes participate in wound repair, particularly the matrix metalloproteinases. We hypothesize macrophage metalloelastase (MME/MMP-12) deficiency results in impaired healing of MCL injury. One hundred fifty MME-deficient and 150 WT (MME+/+) mice underwent knee MCL transection with the opposite knee as a sham operated control. Mice were sacrificed at 3, 7, 28, 42, and 56 days. At each of the five time points, 15 mice were utilized for biological and 15 were utilized for biomechanical testing. Outcome measures were the presence of macrophages to represent the inflammatory phase of wound healing, collagen synthesis to assay for matrix repair, and biomechanical testing for repair strength. Immunohistochemistry demonstrated significantly fewer macrophages in cut MCLs from MME-deficient mice versus wild-type (WT) mice at 3, 7, 28, and 42 days (all p<or=0.04). In situ hybridization to Col1a1 mRNA in the MME-deficient cut MCLs at 7, 28, and 42 day time points showed a decreased level of type I pro-collagen mRNA compared to the WT cut MCLs (p<0.05). Biomechanical testing revealed cut ligaments from MME-deficient mice had significantly lower ultimate force and stiffness compared to cut ligaments from WT mice (p<0.001), with maximal differences of 40% at 7 days for ultimate force and 28 days for stiffness (p<0.05 by Tukey post hoc test). We conclude MME is important in the multifactorial cascade of knee MCL injury healing, showing significant differences in both the early inflammatory and in the matrix tissue synthesis phases.

Animals↗
PubMed2006

Bucket handle tears of the medial meniscus: meniscal intrusion rather than meniscal extrusion.

OBJECTIVE: To determine the frequency of medial meniscal extrusion (MME) versus "medial meniscal intrusion" in the setting of bucket handle tears. Images were evaluated for previously reported risk factors for MME, including: medial meniscal root tear, radial tear, degenerative joint disease and joint effusion. METHODS: Forty-one consecutive cases of bucket handle tear of the medial meniscus were reviewed by consensus by two musculoskeletal radiologists. Imaging was performed using a 1.5 GE Signa MR unit. Patient age, gender, medial meniscal root integrity, MME, medial meniscal intrusion, degenerative joint disease, effusion and anterior cruciate ligament (ACL) tear were recorded. RESULTS: Thirteen females and 27 males (age 12-62 years, median=30 years) were affected; one had bucket handle tear of each knee. Effusion was small in 13, moderate in 9 and large in 18. Degenerative joint disease was mild in three, moderate in two and severe in one. 26 ACL tears included three partial and three chronic. Medial meniscal root tear was complete in one case and partial thickness in two. None of the 40 cases with an intact or partially torn medial meniscal root demonstrated MME. MME of 3.1 mm was seen in the only full-thickness medial meniscal root tear, along with chronic ACL tear, moderate degenerative joint disease and large effusion. Medial meniscal intrusion of the central bucket handle fragment into the intercondylar notch was present in all 41 cases. CONCLUSION: Given an intact medial meniscal root in the setting of a "pure" bucket handle tear, there is no MME.

Adolescent↗
PubMed2005

Mitral annular motion as a surrogate for left ventricular function: correlation with brain natriuretic peptide levels.

BACKGROUND: Pulsed-wave (PW) Doppler tissue velocities of the mitral annulus correlate well with Left Ventricular (LV) diastolic(D) and systolic(S) functions. Brain natriuretic peptide (BNP) levels have been shown to be elevated in patients with symptomatic LV dysfunction (Dys) and correlate to the severity of symptoms and prognosis. OBJECTIVES: To validate the accuracy of mitral annular motion (MAM) assessed by Doppler Tissue Imaging (DTI) & M-mode Echocardiography (MME) as a surrogate for determination of LV function in comparison with BNP. METHODS: A series of 133 patients with a variety of cardiac pathologies referred for echocardiography and 20 healthy age & sex matched volunteers as a control group were included the study. Ejection fraction (EF) of LV, Doppler recordings of the mitral inflow, MME and PWDTI data (from each of 4 mitral annular sites, inferior, anterior, septum and lateral) were obtained. Mean peak (S) MAM velocity (Sm), mean annular early (D) velocity (Em) by PWDTI and mean mitral annular plane (S) excursion (MAPSE) by MME were calculated by averaging of values measured at each annular site. BNP levels were measured by a rapid immunoassay and blinded to cardiologist making the assessment of LV function. RESULTS: MAPSE < 12 mm determined by MME has 90% sensitivity, 88% specificity & 89% accuracy for detection of LVEF <50%, while these values were 94%, 93% & 94% respectively for (Sm) < 8 cm/s determined by PWDTI. BNP level>75 pg/ml has 98% sensitivity, 90% specificity & 97% accuracy for detection of LV Dys either (S,D, or both). BNP levels were significantly higher in patients with combined (S & D) Dys. Than those with only (S) Dys, the later group had significantly higher BNP levels than those with only (D) Dys. (1054.5 +/- 202.3 pg/ml vs. 500 +/- 39.9 pg/ml & 500 +/- 39.9 pg/ml vs. 215.3 +/- 100.9 pg/ml respectively, P < 0.001) & each were significantly higher than control group (12.3 +/- 5.7 pg/ml, P < 0.001). Significant correlations (P < 0.001 for all) were found between BNP levels and Em (r =-0.82), Sm (r=-0.7), early transmitral (E) to Em ratio (r=0.61), MAPSE (r=-0.54), LVEF(r=-0.64) & LV end D dimension (r=0.63). CONCLUSION: MME and PWDTI used for assessment of MAM are useful methods for evaluation of LV function but parameters measured by PWDTI correlate more strongly with plasma BNP levels than those measured by MME and provide a simple, sensitive, accurate and reproducible tool for early diagnosis of LV dysfunction.

Analysis of Variance↗