Correlation was positive between the G+C content at the codon third position in genes of vertebrates and the G+C content of the genome portion surrounding each gene. Exons of genes with a high G+C% ...at the codon 3rd position are surrounded by G+C-rich introns and G+C-rich flanking sequences, and those with a low G+C% at the position by A+T-rich introns and flanking sequences. Analysis of G+C content distribution along DNA sequences using a DNA Sequence Data Bank supported the view that the vertebrate genome is a mosaic of regions with clear differences in their G+C content. biological significance of thevariation in G+C content throughout the vertebrate genome is discussed in connection with chromosomal banding.
In this study we have examined for molecular heterogeneity of cell-matrix adhesions and the involvement of actomyosin contractility in the selective recruitment of different plaque proteins. For this ...purpose, we have developed a novel microscopic approach for molecular morphometry, based on automatic identification of matrix adhesions, followed by quantitative immunofluorescence and morphometric analysis. Particularly informative was fluorescence ratio imaging, comparing the local labeling intensities of different plaque molecules, including vinculin, paxillin, tensin and phosphotyrosine-containing proteins. Ratio imaging revealed considerable molecular heterogeneity between and within adhesion sites. Most striking were the differences between focal contacts, which are vinculin- and paxillin-rich and contain high levels of phosphotyrosine, and fibrillar adhesions, which are tensin-rich and contain little or no phosphotyrosine. Ratio imaging also revealed considerable variability in the molecular substructure of individual focal contacts, pointing to a non-uniform distribution of phosphotyrosine and the different plaque constituents. Studying the quantitative relationships between the various components of the submembrane plaque indicated that the levels of vinculin, paxillin and phosphotyrosine in adhesion sites are positively correlated with each other and negatively correlated with the levels of tensin. Tyrosine phosphorylation of focal contacts was highly sensitive to cellular contractility, and was diminished within 5 minutes after treatment with the kinase inhibitor H-7, an inhibitor of actomyosin contractility. This was followed by the loss of paxillin and vinculin from the focal adhesions. Tensin-rich fibrillar adhesions were relatively insensitive to H-7 treatment. These findings suggest a role for contractility in the generation of matrix adhesion diversity.
The binding of fibronectin (Fn) to several integrins involves the Arg-Gly-Asp (RGD) tripeptide sequence. However, linear synthetic
RGD peptides do not completely mimic the cell attachment activity of ...intact Fn or certain large Fn fragments. This suggests
that the integrin-Fn interaction involves a more extended surface of Fn than that provided by the RGD sequence. To test this
possibility, three novel monoclonal anti-Fn antibodies that inhibit its binding to a purified integrin, alpha IIb beta 3,
were developed. The epitopes of these three antibodies mapped to a region at least 55 residues amino-terminal of the RGD sequence.
Further, recombinant fragments of Fn containing these epitopes and lacking the RGD site also inhibited the binding of Fn to
purified alpha IIb beta 3. These fragments, which spanned Fn residues 1359-1436, bound to alpha IIb beta 3 in a divalent cation-dependent
manner. In addition, this region of Fn bound specifically to alpha IIb beta 3 on thrombin-stimulated but not resting platelets.
These results demonstrate the presence of additional sequences in Fn that interact with integrin alpha IIb beta 3 and suggest
that multiple sites in Fn are involved in its recognition by this integrin.
AISI 317 L stainless steel replaces 316 L grade in some applications due to its superior mechanical strength and corrosion resistance. Aiming at expanding its applicability to structural ...applications, ongoing studies are dedicated to overcoming the trade-off between strength and ductility. The stacking fault energy decreases with deformation temperature and favors stacking faulting, (nano)twinning and strain-induced martensite (SIM) formation, resulting in severe microstructural fragmentation. The effect of temperature on deformation behavior of AISI 317 L steel was investigated in samples rolled at room temperature to thickness reductions of 50% and 85% and at 77 K to reductions in thickness of 10% and 50%. The microstructural evolution was followed by scanning electron microscopy, Vickers microhardness, X-ray diffraction, magnetization, electron backscatter diffraction (EBSD) and electron channeling contrast imaging (ECCI). The nucleation sites in the early stages of the transformation sequence γ → ε → α’ were identified in the 10% cryorolled sample. The highest volume fraction of α’-martensite reached 45.8% in the cryorolled steel to 50% rolling reduction. Much lower fractions were obtained for samples rolled to 10% reduction at 77 K (2%) and at room temperature to 50% (0.3%) and 85% reductions (1.6%). The texture components after cryorolling were Goss and Brass for austenite; rotated cube, α- and γ-fibers for δ-ferrite and α’-martensite. The ε-martensite presents the typical texture of hcp metals with a c/a ratio above the ideal value and 〈0001〉 − oriented tilted about 21° from the normal direction towards the rolling direction. The results show cryorolling as an effective method for enhancing SIM formation and promoting severe microstructural refinement in AISI 317 L stainless steel.
Cryorolling at 77 K favors strain-induced martensite formation. Display omitted
•Cryorolling at 77 K favors the formation of strain-induced martensite (SIM).•Dislocation slip and twinning are the main deformation mechanisms during rolling at RT.•KAM analysis indicates an equivalent strain partitioning among the phases.•Magnetic measurements quantified the volume fraction of α’-martensite.•The volume fraction of ε- and α’-martensite increases with strain.
We examined the bone turnover and bone mass in adjuvant-induced arthritis in rats and assessed the effects of indomethacin in this model. One hundred ten SD rats, 6 weeks of age, were assigned to 11 ...groups and injected with adjuvant or solvent in the right foot. Adjuvant-injected rats were orally administered indomethacin at doses of 0 (vehicle), 0.1 (low), 0.5 (medium), and 1.5 (high) mg/kg body weight from the start (day 0). Animals were sacrificed on days 0, 14 (acute phase), and 28 (chronic phase). In the arthritic-control group, serum osteocalcin level and bone mineral content of the fourth lumbar body (L4) and the femur were significantly reduced on day 14. Serum alkaline-phosphatase was increased on day 28. Trabecular bone volume of L4 was decreased on day 14, and the value was further decreased on day 28. Bone formation rate (BFR/BS) was significantly reduced on day 14, and then osteoclast number (Oc.N/BS) increased on day 28. Indomethacin treatment dose-dependently prevented increases in paw volume and osteoclast number. In the high dose group, these indices were maintained at the same level with those in the normal group. However, indomethacin treatments were not able to maintain the parameters of bone formation such as serum osteocalcin and BFR/BS values, and the trabecular bone mass decrease was only partially prevented. These data clearly indicated both reduced bone formation and increased bone resorption as the causes of bone loss in adjuvant-induced arthritis in rats. Increased bone resorption seemed to be due to the increased activity of prostaglandins, but bone formation defect would be related to other factors in this animal model.
We examined the effects of prednisolone (PSL) administration in normal female Sprague Dawley rats and adjuvant-induced arthritic rats at the age of 6 weeks. Rats were intramuscularly injected with ...PSL twice a week at doses of 0 (control), 10, 30, 90, or 270 mg/kg body weight (b.w.). In the normal rats, serum osteocalcin level at 14 days and serum carboxyterminal pyridinoline cross-linked telopeptide of type 1 collagen (1CTP) level at 28 days in the 270 mg/kg dose group was lower than the respective value in control animals. The BMC and the trabecular bone formation rate (BFR/BS) of the lumbar body (L-4) in the 270 mg/kg dose group at 14 and 28 days were significantly lower than the values in the control rats. In the arthritic rats, however, serum osteocalcin levels in the PSL-treated groups did not differ compared with arthritic controls. The serum 1CTP levels in all of the PSL-treated groups were significantly reduced at 28 days. The age-dependent increases in the L-4 BMC, BMD, and L-3 ultimate compressive load values were maintained. The BFR/BS values in the 90 mg/kg and 270 mg/kg dose groups were significantly higher than those in the arthritic control rats. The trabecular osteoclast number and surface values in all of the PSL-treated groups were significantly lower than the values in arthritic controls. These data demonstrate that PSL administration prevented reduction in bone mass and strength of the lumbar trabecular bone in adjuvant-induced arthritic rats by reducing the increase in bone resorption and the decrease in bone formation at both the local and systemic levels.
Intercalibration of the longitudinal segments of a calorimeter system Albrow, M; Aota, S; Apollinari, G ...
Nuclear instruments & methods in physics research. Section A, Accelerators, spectrometers, detectors and associated equipment,
07/2002, Letnik:
487, Številka:
3
Journal Article
Recenzirano
Three different methods of setting the hadronic energy scale of a longitudinally segmented calorimeter system are compared with each other. The merits of these methods have been studied with testbeam ...data from the CDF Plug Upgrade Calorimeter. It turns out that one of the (commonly used) calibration methods introduces a number of undesirable side effects, such as an increased hadronic signal nonlinearity and trigger biases resulting from the fact that the reconstructed energy of hadrons depends on the starting point of their showers. These problems can be avoided when a different calibration method is used. The results of this study are applied to determine the
e/
h values of the calorimeter and its segments.
We examined the effects of low doses methotrexate (MTX) and indomethacin (IND) on bone mass and turnover in normal male Sprague-Dawley rats and those with adjuvant-induced arthritis. Normal and the ...adjuvant (heat-killed mycobacterium)-injected rats, 6 weeks of age, were given MTX at daily doses of 0.05, 0.1, or 0.2 mg/kg body weight (BW) or IND at a daily dose of 1.0 mg/kg BW. Rats were killed at the start, or at 14 and 28 days. In normal rats, the administration of these agents did not change the lumbar and femoral BMD values, nor did the serum osteocalcin or urinary deoxypyridinoline (D-Pyr) levels. Lumbar trabecular osteoclast number (Oc.N/BS) and osteoclast surface (Oc.S/BS) were decreased in the rats given IND. In the arthritic rats, the administration of MTX did not prevent an early increase of paw edema in the adjuvant-injected limb, but late inflammatory edema was alleviated in the non-injected limb. However, MTX administration at a dose of 0.1-0.2 mg/kg BW maintained an age-dependent increase in the lumbar and femoral BMD values. While serum osteocalcin levels were decreased and urinary D-Pyr values were increased in the arthritic control rats, these bone markers remained at the levels of the normal rats. Decreases in mineral apposition rate (MAR) and bone formation rate (BFR/BS) and increases in the trabecular Oc.N/BS and Oc.S/BS values were prevented by MTX. While IND almost completely prevented inflammatory paw edema, it did not improve the parameters of bone formation. An increase in osteoclasts was prevented and the osteopenia in the lumbar and the femoral bone was only partially prevented by IND. These data suggest that MTX improves bone mass and turnover in the arthritic rat, in which several cytokines that affect bone cells are involved. An increase in bone resorption may be due to prostaglandins, but bone formation defect was suggested to be due to other cytokines such as IL-1, IL-6, and TNF-alpha in this model.