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Matrix metalloprotein ase expression increases after cerebral focal ischemia in rats: inhibition of matrix metalloprotein ase-9 reduces infarct size.: Stroke, Vol. 29, No. 5. (May 1998), pp. 1020-1030.BACK GROUND AND PURPOSE: Matrix metalloprotein ases (MMPs) are a family of proteolytic enzymes that degrade the extracellular matrix and are implicated in numerous pathological conditions including atherosclerosi s, inflammation, and tumor growth and metastasis. In the brain, the endothelial cell wall, strengthened by tight junctions, defines the blood-brain barrier (BBB). The extracellular matrix molecules constitute the basement membrane underlying the vasculature and play a critical role in maintaining the integrity of the BBB. After focal stroke, there is a breakdown of the BBB with an associated increase in vascular permeability, inflammatory cell influx, and neuronal cell death. The present study was designed to investigate the effects of MMP expression after stroke. METHODS: Focal stroke was produced by permanent middle cerebral artery occlusion (MCAO) in the rat, and MMP protein expression was measured by Western blot and zymogram analysis over a time course ranging from 6 hours to 30 days (n=32). Immunohistoche mistry at 1 and 5 days (n=8 and 6, respectively) was also utilized to characterize the expression of several MMPs and related proteins after stroke, including their cellular source. To test the hypothesis that early increased MMP-9 expression is involved in ischemic brain injury, a neutralizing monoclonal antibody directed against MMP-9 was administered intravenously (n=7 per group) 1 hour before MCAO, and infarct size was measured 24 hours later. RESULTS: MMP expression increased progressively over time after stroke. After 12 hours, significant (P

Source: Stroke, Vol. 29, No. 5. (May 1998), pp. 1020-1030.
Average Liouvillian theory in nuclear magnetic resonance - Pr inciples, properties, and applications: Concepts in Magnetic Resonance, Vol. 12, No. 3. (2000), pp. 152-172.The transient as well as the long-term behavior of the spin-density operator under the influence of radiofrequency pulses and periods of free-precessio n can be predicted to a reasonable degree of accuracy within the framework of the Average Liouvillian Theory. This approach can be used to design pulse sequences which suppress the effects of certain components of the Liouvillian on the spin dynamics while allowing the detailed analysis of the effects of others. We present here the basic principles of Average Liouvillian Theory and its application in the design of pulse sequences to study the structural and dynamic properties of biomolecules. © 2000 John Wiley & Sons, Inc. Concept s Magn Reson 12: 152-172, 2000

Source: Concepts in Magnetic Resonance, Vol. 12, No. 3. (2000), pp. 152-172.
Fairness and Envy: The American Economic Review, Vol. 64, No. 6. (1974), pp. 995-1005.

Source: The American Economic Review, Vol. 64, No. 6. (1974), pp. 995-1005.
Development of Semantic Web Services at the Knowledge Level: Lecture Notes in Computer Science : Web Services (2004), pp. 72-86.

Source: Lecture Notes in Computer Science : Web Services (2004), pp. 72-86.
Liver enzyme values in injection drug users with chronic hepatitis C.: Dig Liver Dis (9 June 2005)BACKGROUN D.: Liver enzymes fluctuate in chronic hepatitis C virus infection. However, the range that can be attributed to the course of hepatitis C virus (versus an intercurrent cause of hepatitis) is unknown. AIMS.: To characterise the range of liver enzyme values as a function of the upper limit of normal (ULN) of the assay among persons chronically infected with hepatitis C virus. PATIENTS.: One thousand and fifty-nine hepatitis C virus chronically infected individuals with >/=5 semi-annual evaluations. METHODS.: Alanine aminotransfera se and aspartate aminotransfera se levels were prospectively obtained. Potential causes of elevations were examined using serologic testing. RESULTS.: Among 1059 individuals, 11,463 enzyme measurements were obtained over 6.5 years, of which 63.5% were 10x ULN. Elevations >10x ULN were transient, the alanine aminotransfera se/aspartate aminotransfera se ratio tended to be different at the time of the elevation compared to before and after and 24% were associated with acute viral hepatitis. On the other hand, subjects with elevations 5-10x ULN tended to have elevated levels throughout follow-up and only 8% were associated with acute viral hepatitis. CONCLUSIONS.: Liver enzymes fluctuate up to 5x ULN in most hepatitis C virus-infected persons; clinicians should seek alternate explanations for those with higher alanine aminotransfera se or aspartate aminotransfera se levels, especially among hepatitis C virus-infected persons with greater than 10-fold elevations.

Source: Dig Liver Dis (9 June 2005)
NF90 regulates cell cycle exit and terminal myogenic differentiatio n by direct binding to the 3'-untranslate d region of MyoD and p21WAF1/CIP1 mRNAs.: J Biol Chem, Vol. 280, No. 19. (13 May 2005), pp. 18981-18989.NF 90 and splice variant NF110/ILF3/NFA R are double-strande d RNA-binding proteins that regulate gene expression. Mice with targeted disruption of NF90 were engineered. NF90(-/-) mice were born small and weak and succumbed to perinatal death within 12 h because of neuromuscular respiratory failure. Lung inflation and morphology were normal in NF90(-/-) mice. The diaphragm and other skeletal muscles in NF90(-/-) mice demonstrated disorganized arrangement and paucity of myofibers, evidence of myocyte degeneration and increased apoptosis. The expression of myogenic regulators, MyoD, myogenin, and p21WAF1/CIP1, was severely decreased in NF90(-/-) mice. These myogenic transcription factors and cell cycle inhibitors are regulated in part through post-transcrip tional mRNA stabilization. Northwestern blotting revealed that NF90 is the principal and specific p21WAF1/CIP1 and MyoD 3'-untranslate d region RNA-binding protein in developing skeletal muscles. NF90 regulates transcription factors and a cell cycle inhibitor essential for skeletal muscle differentiatio n and for survival.

Source: J Biol Chem, Vol. 280, No. 19. (13 May 2005), pp. 18981-18989.
Role of the Fetal and alpha/beta Exons in the Function of Fast Skeletal Troponin T Isoforms: Correlation with Altered Ca(2+) Regulation Associated with Development.: J Mol Biol (1 August 2005)In mammalian fast skeletal muscle, constitutive and alternative splicing from a single troponin T (TnT) gene produce multiple developmentall y regulated and tissue specific TnT isoforms. Two exons, alpha (exon 16) and beta (exon 17), located near the 3' end of the gene and coding for two different 14 amino acid residue peptides are spliced in a mutually exclusive manner giving rise to the adult TnTalpha and the fetal TnTbeta isoforms. In addition, an acidic peptide coded by a fetal (f) exon located between exons 8 and 9 near the 5' end of the gene, is specifically present in TnTbeta and absent in the adult isoforms. To define the functional role of the f and alpha/beta exons, we constructed combinations of TnT cDNAs from a single human fetal fast skeletal TnTbeta cDNA clone in order to circumvent the problem of N-terminal sequence heterogeneity present in wild-type TnT isoforms, irrespective of the stage of development. Nucleotide sequences of these constructs, viz. TnTalpha, TnTalpha+f, TnTbeta-f and TnTbeta are identical, except for the presence or absence of the alpha or beta and f exons. Our results, using the recombinant TnT isoforms in different functional in vitro assays, show that the presence of the f peptide in the N-terminal T1 region of TnT, has a strong inhibitory effect on binary interactions between TnT and other thin filament proteins, TnI, TnC and Tm. The presence of the f peptide led to reduced Ca(2+)-depende nt ATPase activity in a reconstituted thin filament, whereas the contribution of the alpha and beta peptides in the biological activity of TnT was primarily modulatory. These results indicate that the f peptide confers an inhibitory effect on the biological function of fast skeletal TnT and this can be correlated with changes in the Ca(2+) regulation associated with development in fast skeletal muscle.

Source: J Mol Biol (1 August 2005)
Alternative pre-mRNA splicing governs expression of a conserved acidic transactivatio n domain in myocyte enhancer factor 2 factors of striated muscle and brain.: J Biol Chem, Vol. 280, No. 31. (5 August 2005), pp. 28749-28760.My ocyte enhancer factor 2 (MEF2) transcription factors play pivotal roles in striated muscle, neuron, and lymphocyte gene expression and are targets of stress- and calcium-mediat ed signaling. All MEF2 gene products have a common DNA binding and dimerization domain, but MEF2 transcripts are alternatively spliced among coding exons to produce splicing isoforms. In vertebrate MEF2A, -C, and -D, a splice versus no-splice option gives forms that include or exclude a short domain that we designate beta. We show that mRNAs containing beta are expressed predominantly in striated muscle and brain and that splicing to include beta is induced during myocyte differentiatio n. MEF2 beta+ isoforms are more robust than beta- forms in activating MEF2-responsiv e reporters despite similar expression levels. One-hybrid transcription assays using Gal4-MEF2 fusions show similar distinctions in the transactivatio n produced by beta+ versus beta- isoforms in all cell types tested, including myocytes. beta function is position-indep endent and exists in all MEF2 splicing variant contexts. The activity is not due to cis effects on MEF2 DNA binding or dimerization nor are established transcription factor or coactivator interactions involved. Each MEF2 beta domain contains multiple acidic residues, mutation of which abolishes function. Despite a location between the p38 MAPK docking domain and Thr phosphoaccepto rs of MEF2A and MEF2C, inclusion of beta does not influence responses of these factors to this signaling pathway. Thus, a conserved pattern of alternative splicing in vertebrate MEF2 genes generates an acidic activation domain in MEF2 proteins selectively in tissues where MEF2 target genes are highly expressed.

Source: J Biol Chem, Vol. 280, No. 31. (5 August 2005), pp. 28749-28760.
The social cost of cheap pseudonyms: (1998)We consider the problems of societal norms for cooperation and reputation when it is possible to obtain "cheap pseudonyms", something which is becoming quite common in a wide variety of interactions on the Internet. This introduces opportunities to misbehave without paying reputational consequences. A large degree of cooperation can still emerge, through a convention in which newcomers "pay their dues" by accepting poor treatment from players who have established positive reputations. One might ...

Source: (1998)
Evidence for an alternative mechanism for maintaining telomere length in human tumors and tumor-derived cell lines.: Nat Med, Vol. 3, No. 11. (November 1997), pp. 1271-1274.The gradual loss of DNA from the ends of telomeres has been implicated in the control of cellular proliferative potential. Telomerase is an enzyme that restores telomeric DNA sequences, and expression of its activity was thought to be essential for the immortalizatio n of human cells, both in vitro and in tumor progression in vivo. Telomerase activity has been detected in 50-100% of tumors of different types, but not in most normal adult somatic tissues. It has also been detected in about 70% of human cell lines immortalized in vitro and in all tumor-derived cell lines examined to date. It has previously been shown that in vitro immortalized telomerase-neg ative cell lines acquire very long and heterogeneous telomeres in association with immortalizatio n presumably via one or more novel telomere-lengt hening mechanisms that we refer to as ALT (alternative lengthening of telomeres). Here we report evidence for the presence of ALT in a subset of tumor-derived cell lines and tumors. The maintenance of telomeres by a mechanism other than telomerase, even in a minority of cancers, has major implications for therapeutic uses of telomerase inhibitors.

Source: Nat Med, Vol. 3, No. 11. (November 1997), pp. 1271-1274.

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