Using ultrasound measurements of the femur, tibia, humerus, radius (N = 515), and fibula and ulna (N = 385) from normal fetuses between 12 and 40 completed weeks of gestation, growth models were determined for each bone by computer analysis. On the basis of residual analysis, growth of fetal limb bones could best be expressed as a function of tangens hyperbolicus. Growth profiles and growth data are shown with 5th, 10th, 50th, 90th, and 95th percentiles. These results are compared with previous investigations of limb bone measurements.

Bone and Bones↗

PubMedDate not supplied

Binase does not induce polyclonal T-cell response.

Explore the source record for details and available documents.

Antineoplastic Agents↗

PubMedDate not supplied

Morphogenic effects of endothelin-1 on vascular smooth muscle cells.

Endothelin-1 (ET-1), a vasoconstrictor peptide produced by endothelial and vascular smooth muscle cells (VSMC) might play a role in vascular remodelling. To investigate the proposed 'mitogenic' potential of ET-1, we examined the effects of chronic exposure of VSMC to ET-1 on cell cycle, growth/proliferation and differentiation under essentially mitogen-free culture conditions. Bulk cultures of thoracic aortic VSMC of spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats, although exhibiting genetically determined differences in growth/proliferation (due to shortened G1 and G2 phases in SHR VSMC), respond in a similar manner to ET-1 exposure: long-term exposure (12-15 days) of VSMC from both sources to ET-1 in nonmitogenic medium did not promote cycling of cells. On the contrary, ET-1 attenuated the cycling of VSMC which had already cycled beyond the S phase. For cells which had not cycled beyond the S phase, ET-1 interrupted progression through the cell cycle at the late G1/early S phase. The specific ability of SHR VSMC to grow in mitogen-free medium was abolished by ET-1, most likely via down-regulation of platelet-derived growth factor (PDGF)-alpha receptors. Subsequent to ET-1 exposure, VSMC expressed increased levels of mRNA and protein for smooth-muscle-specific alpha-actin. However, expression of smooth muscle alpha-actin did not predominate over beta-actin as observed for adult contractile VSMC in vivo. The ET-1-induced expression of smooth-muscle-specific alpha-actin mRNA was dose dependent (EC50 approx. 2 x 10(-9) M), and alpha-actin protein expressed was associated with organized actin fibers.

Actins↗

PubMedDate not supplied

Angiotensin-II-induced expression of laminin complex and laminin A-chain-related transcripts in vascular smooth muscle cells.

Laminin, a major structural glycoprotein complex of basement membranes has been found to be modulated by angiotensin II in vitro and in vivo. In cultures of aortic organoids and vascular smooth muscle cells, expression of laminin was stimulated by exogenous vasoconstrictor peptide. Stimulation of laminin protein and mRNA expression was observed for both laminin B1/B2-chains and an unknown laminin heavy chain. Compared with PYS-2 cells, a mouse teratocarcinoma cell line which constitutively expresses a 10-kb mRNA transcript for 'classical' laminin A-chain, cultured vascular smooth muscle cells (VSMC) did not express a corresponding mRNA. However, cultured VSMC were found to express laminin A-chain-related mRNAs of approximately 1.8 kb and approximately 3.8 kb, respectively. The 1.8-kb species of transcript was expressed in a constitutive manner, whereas the 3.8-kb mRNA was found to be regulated by angiotensin II. Laminin complexes secreted by cultured cells contained a approximately 300 kD heavy chain which did not immunoreact with immunoreagents raised against either the classical laminin complex secreted by EHS tumor cells or the merosin heavy chain. The putative A-chain analogue possibly represents a new form of a tissue-specific laminin heavy chain, distinct from the A- and M-chains thus far described. Translation products encoded by the A-chain-related transcripts of cultured smooth muscle cells could not be specified using currently available antibodies. The putative protein(s) is speculated to contain the biological features of the N-terminus of the laminin A-chain, namely self-assembly and association with collagen type IV.

Animals↗

PubMedDate not supplied

Functional aspects of vascular tenascin-C expression.

The arterial tenascin C expression in vivo and in vitro has been studied using immunohistochemistry. The functional relevance of localized tenascin C expression was assessed in vitro using various human cell types involved in the progression of vascular disease. Normotensive and hypertensive rats exhibited age-dependent patterns of vascular (aorta) tenascin expression, but the lumen-to-media-directed progression of tenascin induction was accelerated in hypertensive rats. Tenascin-rich neointimal lesions (spontaneous) were observed at branching sites of aorta from aged (80 weeks) hypertensive rats. Subendothelial tenascin foci contained lipid-laden smooth muscle cells and monocytes/macrophages. Medial tenascin foci encaged smooth muscle cells which synthesized DNA. Tenascin was expressed both in vivo and in vitro by endothelial and smooth muscle cells but not by monocytes/macrophages; angiotensin II, oxidized-low density lipoprotein and transforming growth factor beta 1 induced expression of tenascin transcripts and glycoprotein in vitro. Endothelial and smooth muscle cells, but not monocytes, adhered to tenascin substrata. Tenascin reduced focal adhesion integrity in confluent endothelial and smooth muscle cell cultures. Angiotensin II-induced migration of endothelial and smooth muscle cells was accompanied by tenascin deposition within extracellular matrix migration trails. Tenascin may function both as a defense against monocyte invasion and medial smooth muscle replication, as well as a substratum for directed endothelial and smooth muscle cell migration.

Animals↗

PubMedDate not supplied

[Xymedon decreases phosphatidylserine membrane expression induced by proapoptogenic deficit of serum growth factors in Jurkat T-cells].

The effect of xymedone, a non-glucoside analog of pyridine nucleosides, on the apoptosis of human CD4+ T cells of the Jurkat line was studied by laser flow cytometry method. Xymedone decreased the membrane expression of phosphatidylserine and suppressed the increase in permeability of the cytoplasmic membrane, thus inhibiting the onset of a degradation stage of the apoptotic cascade. Possible mechanisms of the antiapoptogenic effect of xymedone within the framework of a (cytochrome C/caspase 3)-dependent signal pathway of the apoptosis are discussed.

Apoptosis↗

PubMedDate not supplied

A protocol for combining proliferation, tetramer staining and intracellular cytokine detection for the flow-cytometric analysis of antigen specific T-cells.

Flow-cytometry can be used in different ways in order to analyze or enumerate antigen specific T-cells. The three basic principles are direct staining of the T-cell receptor using so called tetramer reagents, staining intracellular cytokines following antigen-specific ex vivo T-cell activation or staining with dyes that are incorporated (increase in staining) or distributed between daughter cells (decrease in staining) upon proliferation in response to a specific antigen challenge. Each system has its advantages and disadvantages. Here we demonstrate that tetramer staining, cytokine flow cytometry and staining with CFDA-SE can be combined permitting the analysis of proliferation and cytokine production with a subset of T-cells specific for a single peptide antigen.

Antigens↗