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Biomedical subjects

M Rahm

Publications and source records attributed to M Rahm.

12 recordsLinked to original sources

Shifting and pinning of a magnetic vortex core in a permalloy dot by a magnetic field.

Magnetic pinning in thin films seems to be a major research subject in the near future, as it is involved in all switching processes which include a movement of a domain wall or a magnetic vortex. We used Lorentz transmission electron microscopy and vortex pinning at artificial pinning sites to investigate the pinning behavior of magnetic vortices for the first time with high spatial resolution.

Journal Article↗

Fatigue in the shoulder muscles during static work at two different torque levels.

The present study aimed to investigate whether and when a shift in the mean power frequency (MPF) of the electromyogram (EMG) occurs at low torque levels during a maximum endurance test of three shoulder flexors. Twelve clinically healthy women performed two endurance tests of the shoulder flexors (at 50% MVC--the high torque level, and at approximately 18% MVC--the low torque level) until maximum exhaustion. Surface EMG were obtained and MPF and signal amplitude (RMS) were computed for the trapezius descendens, the anterior part of the deltoid and the infraspinatus. The subjects also rated the perception of fatigue in the shoulder muscles throughout the two tests using a 10-graded scale. A significantly higher degree of perceived fatigue was found at the low rather than at the high torque level. In contrast significantly lower MPF were found at the end of the endurance times in the three muscles at the high torque level when compared to the low torque level. At the low torque level MPF of the trapezius was constant throughout the test. In the deltoid the most prominent decrease occurred during the initial 30-40% of the endurance time at the low torque level. It is suggested that the MPF shift mainly reflects peripheral fatigue of the type-2 fibres. The results of the present study question the use of the MPF shift to monitor peripheral fatigue in the fibres active (mainly type-1) at low torque levels.

Adult↗

Neurokinin A induces c-fos, c-jun, and c-myc expression in L6 rat myoblasts.

Neurokinin A (NKA), a neuropeptide belonging to the tachykinin family, induced c-fos proto-oncogene mRNA expression in serum-deprived L6J1 rat skeletal myoblasts in vitro. The marked increase reached maximal levels after 15 to 30 min. In contrast to this, c-jun and c-myc proto-oncogene expression were only slightly induced, with peak levels after 30 min. NKA did not stimulate DNA synthesis or cell proliferation in serum-deprived L6J1 myoblasts. We demonstrate a relationship between NKA treatment and induction of c-fos, c-jun and c-myc mRNA expression in serum-deprived L6J1 rat myoblasts. The results on DNA synthesis and cell proliferation indicate that the induced proto-oncogene expression alone is not enough to induce a cellular response to NKA. Possible mechanisms of action are discussed.

Animals↗

c-fos reduces growth factor requirements for mitogenic stimulation of L6 rat myoblasts.

Addition of fetal calf serum (FCS) to serum-deprived L6J1 rat myoblasts increases fos-like immunoreactivity. The nuclear immunoreactivity reached a maximum 2 h after serum addition. Effects of the c-fos protein on myoblast proliferation were analyzed in L6J1 rat myoblasts transfected with the murine c-fos gene under control of a metallothionein promoter. L6J1 myoblasts with elevated expression of transfected c-fos reached higher cell densities than neo transfected control myoblasts when approaching a stationary phase in normal culture conditions (5% FCS). The differences in cell densities were even more pronounced at low serum concentrations (0.5% FCS). c-fos transfected cells also had a faster growth rate than did control cells in serum-free medium supplemented with calcium chloride, lithium chloride, sodium selenite, hydrocortisone, and insulin. The cell morphology of c-fos transfected L6J1 myoblasts was not affected compared to control myoblasts. These results suggest that c-fos protein expression in L6J1 myoblasts is activated by serum and that mitogenic stimulation of L6J1 myoblasts is facilitated by the presence of elevated amounts of c-fos protein.

Animals↗

Intracellular distribution of the c-fos antigen during the cell cycle.

The subcellular localization of the c-fos proto-oncogene product was studied in the G1, S, G2, and mitotic phases of the cell cycle by indirect immunofluorescence. For these analyses c-fos transfected L6J1 rat skeletal myoblasts and adult rat aortic smooth muscle cells in secondary culture, and c-fos- and c-myc co-transfected mouse Swiss 3T3 fibroblasts were used. During G1, S, and G2, the c-fos protein was evenly distributed in the nucleus, with exclusion of the nucleoli. In mitotic prophase the c-fos antigen was dissociated from the condensed chromosomes and became diffusely distributed in the cell cytoplasm, where it remained until telophase, when, again, it appeared to be associated with chromatin in the re-assembling nucleus. When comparing the subnuclear distribution of the c-fos product with that of densely packed DNA, stained with the fluorochrome Hoechst, an inverse relationship was found. Dispersed chromatin regions with weak Hoechst DNA fluorescence showed a stronger fos immunofluorescence than regions that contained a higher concentration of DNA. The localization of c-fos antigen partially overlapped with that of antigens typical of small nuclear ribonucleoprotein complexes participating in transcription and splicing. To examine if the c-fos protein would bind preferentially to specific interphase chromosomes the nucleus was fragmented into micronuclei containing single, or groups of, chromosomes. Immunofluorescence analysis showed that the majority of micronuclei were fos-positive. Possible roles of the c-fos proto-oncogene product are discussed in relation to other nuclear antigens.

Animals↗

Expression of PDGF A-chain and beta-receptor genes during rat myoblast differentiation.

L6J1 rat myoblasts and rat skeletal muscle were studied for expression of mRNAs encoding PDGF A-chain, PDGF B-chain, PDGF alpha-receptor, and PDGF beta-receptor during in vitro and in vivo myoblast differentiation. RNA blot hybridizations demonstrated expression of the PDGF A-chain gene and the PDGF beta-receptor gene in L6J1 myoblasts and in crude muscle tissue isolated from developing rats. Transcripts of the PDGF A-chain were identified at all examined stages of in vitro and in vivo myogenic differentiation. Expression of the PDGF beta-receptor gene decreased in differentiated myotubes of L6J1 cells and in rat adult muscle tissue. Receptor binding assays demonstrated specific binding of PDGF-BB, but not -AA, to exponentially proliferating L6J1 myoblasts and to terminally differentiated L6J1 myotubes. The binding per cell nucleus was higher in exponentially proliferating myoblasts than in differentiated L6J1 myotubes. In serum free medium PDGF-BB was shown to increase c-fos protooncogene immunoreactivity in L6J1 myoblasts. In the presence of 0.5% FCS, PDGF-BB increased DNA synthesis in L6J1 myoblasts, while PDGF-AA showed no such effect. Differentiation, as monitored by myotube formation, was reduced in PDGF-BB-treated cultures. The possible role of PDGF in myoblast proliferation and differentiation is discussed.

Animals↗

Expression of PDGF alpha- and beta-receptors in rat arterial smooth muscle cells is phenotype and growth state dependent.

Adult rat arterial smooth muscle cells were shown to express mRNA for the platelet-derived growth factor (PDGF) alpha- and beta-receptors and to bind radioiodinated PDGF-AA and PDGF-BB in a phenotype-dependent and growth state-dependent manner. PDGF alpha-receptor mRNA was not detected in the intact aortic media, but appeared as the cells converted from a contractile to a synthetic phenotype during serum-free primary culture. PDGF beta-receptor mRNA was expressed already in vivo, and increased further as the cells were isolated and cultured in vitro. Exposure of the cells to human platelet PDGF resulted in increased PDGF alpha-receptor mRNA levels, decreased PDGF beta-receptor mRNA levels, and decreased binding of both PDGF-AA and PDGF-BB. Following removal of the exogenous mitogen, the content of PDGF alpha- and beta-receptor mRNA increased, as did the binding of PDGF-AA and PDGF-BB. Subsequently, the content of PDGF A-chain mRNA started to rise, and the cells retained a high rate of DNA synthesis in a serum-free medium. As a result of this autocrine stimulation, the PDGF receptors were down-regulated. Although smooth muscle cells in serum-free primary cultures bound the different PDGF isoforms to a varying extent (AA less than AB less than BB), the replicative response was of a similar magnitude. Subcultured cells bound the different PDGF isoforms in similar proportions as the primary cells. Contrary to the situation in primary cells, there was a direct correlation between the binding level and the DNA synthetic response. Moreover, the subcultured cells did not replicate in a serum-free medium. These observations support the idea that the phenotypic modulation of arterial smooth muscle cells in primary culture prepares the cells to activate autocrine growth mechanisms. When stimulated with an exogenous mitogen, they enter the cell cycle and are thereafter able to stimulate their own growth in an autocrine manner by production of PDGF-AA or a closely related molecule.

Animals↗

Elevated c-fos expression inhibits differentiation of L6 rat myoblasts.

Expression of c-fos is induced by a number of signals in several cell systems. Although the exact function of the c-fos product is unknown, it has been implicated to be of importance for both cell growth and differentiation (Verma and Sassone-Corsi, 1987). To analyze how c-fos expression relates to in vitro myogenic differentiation, the kinetics of c-fos mRNA expression during spontaneous in vitro differentiation of L6J1 myoblasts was examined; c-fos transcripts were most abundant at day 4 of the differentiation process. Multinucleated myotubes and expression of alpha-actin and myosin heavy chain (MHC) mRNA appeared later, at day 6 or 7, and increased to maximal levels after 10 days in culture. To analyze further the relation between c-fos expression and L6J1 myogenic differentiation, L6J1 myoblasts were transfected with expression vectors containing the murine c-fos gene driven by a metallothionein promoter. The growth rate of c-fos-transfected L6J1 cells did not differ from that of control cells. However, formation of myotubes was significantly reduced in c-fos-transfected L6J1 cultures compared with neo-transfected controls. Myotube formation and expression of the myogenic markers alpha-actin and MHC were reduced in subclones expressing high levels of c-fos, but not in subclones with lower levels of c-fos expression. These results indicate that a marked elevation of c-fos expression at least partially inhibits L6J1 myogenic differentiation.

Actins↗

Changes in c-onc expression during embryonal carcinoma cell differentiation.

Protooncogenes expressed in murine embryonal carcinoma (EC) cells or their differentiated daughter cells include more or less ubiquitously expressed protooncogenes such as c-myc, c-K-ras, and c-abl, as well as c-onc genes with a very restricted expression pattern. Examples of the latter are N-myc, c-mos, and int-2. These c-onc genes are transcriptionally active in EC cells, as well as in germ cells and/or early embryonic cells. When EC cells are induced to differentiate some protooncogenes or oncogene-related products undergo changes in expression. Thus, EC cell differentiation has been associated with increased expression of c-src, c-fos, int-1, int-2, and the epidermal growth factor (EGF) receptor, whereas decreased expression has been observed for c-mos, c-K-ras, c-myc, N-myc, and platelet-derived growth factor. The relationships between these changes in expression and EC cell differentiation are not understood. They may be important for the differentiation process or for expression of a differentiated phenotype. They may, however, also be secondary events with no functional significance to EC cell differentiation.

Animals↗

Similarities and differences in the regulation of N-myc and c-myc genes in murine embryonal carcinoma cells.

c-myc and N-myc are closely related genes coding for putative DNA-binding proteins. The protein products of both genes have been implicated in the regulation of growth of normal and neoplastic cells. We compared the regulation of N-myc and c-myc expression under different growth conditions as well as in vitro differentiation of the murine EC lines F9 and PCC7. N-myc and c-myc expression was found to be regulated by distinct mechanisms, although similarities exist. Differences were found both at the transcriptional and at the post-transcriptional level. The two myc genes were regulated by mainly post-transcriptional mechanisms, but in PCC7 cells nuclear run-on assays indicated that c-myc was repressed at the level of transcription. N-myc and c-myc expression was negatively regulated at a post-transcriptional level in F9 and PCC7 cells during differentiation to visceral endoderm and nerve-like tissue, respectively. Serum stimulation of F9 cells for 4 h induced a sevenfold increase in c-myc transcripts but no significant elevation of N-myc transcripts. Mitogenic stimulation with insulin and transferrin also induced a marked elevation of c-myc but not of N-myc mRNA. In addition, the N-myc and c-myc genes differed in F9 cells with respect to (i) the kinetics of expression following induction of differentiation, c-myc undergoing quicker changes than N-myc; (ii) the response to cycloheximide inhibition of protein synthesis, indicating that c-myc but not N-myc is down-regulated by a short-lived protein; and (iii) the half-lives of the transcripts, estimated to be approximately 40 min for c-myc and 130 min for N-myc.

Animals↗

Dennyson-Fulford subtalar arthrodesis.

Forty-six patients who had undergone Dennyson-Fulford subtalar arthrodesis for hindfoot valgus deformities secondary to various pathologies were reviewed both radiographically and clinically. Mean age at surgery was 7.67 years; mean follow-up was 5.67 years. Evaluation showed 70% good, 20% fair, and 10% poor results. Pseudarthrosis rate was 6.4%, and was not necessarily related to undercorrection or progressive deformity. Screw sclerosis, which is common, is associated with pseudarthrosis, but not with hardware failure. Hardware problems can be anticipated with intraoperative radiographs, and penetration of the lateral calcaneal cortex up to 1.0 cm is well tolerated.

Adolescent↗