Objective: To assess the multiexaminer reproducibility and the accuracy comparing with cadaver anatomic specimens of ultrasound (US) measurement of femoral articular cartilage (FAC) thickness. Methods: In 8 flexed cadaver knees, FAC thickness was blindly, independently and consecutively measured twice by 10 rheumatologists at the lateral condyle (LC), medial condyle (MC) and intercondylar notch (IN) with US. After the US measurements, the knees were dissected. Articular cartilage integrity was evaluated macroscopically in the femoral condyles. FAC thickness was blindly measured in the specimens using a stereoscopic magnifying loupe and a digitised image software. Interexaminer and intraexaminer reliability of US FAC thickness measurement and agreement between US and anatomic measurements were assessed by estimating the intraclass correlation coefficient (ICC). Conclusion: US demonstrated a good reproducibility in FAC thickness measurement by multiple examiners. In addition, US FAC thickness measurement was accurate in normal to moderately damaged cartilage.

No abstract

Conde MV, Gonzalez MC, Quintana-Villamandos B, Abderrahim F, Briones AM, Condezo-Hoyos L, Regadera J, Susin C, de Diego JJ, Delgado-Baeza E, Diaz-Gil JJ, Arribas SM. Liver growth factor treatment restores cell-extracellular matrix balance in resistance arteries and improves left ventricular hypertrophy in SHR. Am J Physiol Heart Circ Physiol 301: H1153-H1165, 2011. First published June 3, 2011 doi:10.1152/ajpheart.00886.2010.-Liver growth factor (LGF) is an endogenous albumin-bilirubin complex with antihypertensive effects in spontaneously hypertensive rats (SHR). We assessed the actions of LGF treatment on SHR mesenteric resistance and intramyocardial arteries (MRA and IMA, respectively), heart, and vascular smooth muscle cells (VSMC). SHR and Wistar-Kyoto (WKY) rats treated with vehicle or LGF (4.5 g LGF/rat, 4 ip injections over 12 days) were used. Intra-arterial blood pressure was measured in anesthetized rats. The heart was weighted and paraffinembedded. Proliferation, ploidy, and fibronectin deposition were studied in carotid artery-derived VSMC by immunocytochemistry. In MRA, we assessed: 1) geometry and mechanics by pressure myography; 2) function by wire myography; 3) collagen by sirius red staining and polarized light microscopy, and 4) elastin, cell density, nitric oxide (NO), and superoxide anion by confocal microscopy. Heart sections were used to assess cell density and collagen content in IMA. Left ventricular hypertrophy (LVH) regression was assessed by echocardiography.LGF reduced blood pressure only in SHR. LGF in vitro or as treatment normalized the alterations in proliferation and fibronectin in SHR-derived VSMC with no effect on WKY cells. In MRA, LGF treatment normalized collagen, elastin, and VSMC content and passive mechanical properties. In addition, it improved NO availability through reduction of superoxide anion. In IMA, LGF treatment normalized perivascular collagen and VSMC density, improving the wall-to-lumen ratio. Paired experiments demonstrated a partial regression of SHR LVH by LGF treatment. The effective cardiovascular antifibrotic and regenerative actions of LGF support its potential in the treatment of hypertension and its complications. intramyocardial arteries; mesenteric resistance arteries; nitric oxide; vascular remodeling; left ventricular hypertrophy LIVER GROWTH FACTOR (LGF) was first described as an endogenous factor with mitogenic properties in liver (21).LGF is not detected in physiological conditions, but it increases in plasma in situations of hepato-biliary disorders, both in humans and rats (21,24). The chemical analysis of LGF obtained from human and rat plasma has revealed that it is a covalently bound albumin-bilirubin complex (24,25). The regenerative effects of LGF, initially described in hepato-biliary disorders (22,23,26), have been recently extended to other diseases, such as Parkinson's disease (35, 52), testicular degeneration (51), and pulmonary fibrosis (47).LGF treatment also has cardiovascular effects as previously shown in rodent models of hype...

Adult stem cells are essential for tissue renewal, regeneration and repair, and their expansion in defined culture medium is on focus for regenerative medicine and genetic pathologies. The bone marrow has been shown to be very rich is pluripotent mesenchymal stem cells (MSCs) capable of forming bone, cartilage and also may give rise, to neurons and astrocytes in vivo and in vitro. MSCs can be isolated and expanded in culture, but human cells cannot be verified for a cartilage or a bone fate by transfer experiments. Accordingly, here we used different approaches to characterize hMSCs osteoblastic differentiation in vitro. hMSCs grown in culture in the presence of fetal bovine serum (FBS) expressed the bone-specific transcription factor Runx2/AML3. When cells were incubated in osteoblastic differentiation medium, cells expressed transcripts belonging to the signaling of Indian HH-PTHrP axis, GLI transcription factors, and bone target genes including osteopontin. The HH pathway proved to be functional since it induced cells to grow. Cells growing or differentiating to osteoblasts presented the Runx2/AML3 transcription factor, its partner CBFB, and Smad2/3 at the nuclei associated with the nuclear matrix. Furthermore, Runx2/AML3 was observed to co-localize with SC35 to the nuclear intermediary filaments. These data support the notion that hMSCs isolated from human bone are or become bone progenitor cells upon culture. In the absence of FBS and in the presence of insulin or prolactin, cells show cytoskeletal organization and an AP-1 transcription site activity resembling proliferative osteochondrocytes while cells in the presence of dexamethasone and added prolactin or TGF-beta resembled differentiated osteoblasts. These specific cellular conditions match those observed during endochondral bone formation.