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Fig. 6. Analysis of hearts of mice with deficiencies in the extrinsic pathway of coagulation. Heart sections were stained with Prussian Blue AC ; or Masson's Trichrome D ; . Shown are heart sections from an mTF hTF line 47 ; mouse 12 weeks of age; A ; , an mTF hTF line 31 ; mouse 8 weeks of age; B ; , and an FVIItTA-FVII tTA-FVII mouse 9 weeks of age; C and D.
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Mother was on chronic phenobarbital therapy; Demerol and secobarbital had been administered during labor and delivery. The source of caffeine, which is present in most adult and neonatal urines, was either coffee, tea, cola beverages, or an analgesic preparation ingested by the mother. The drugs and drug metabolites were isolated by the DEAE-Sephadex procedure 1 ; . The drugs identified in the neonatal and maternal urines were caffeine, Demerol, and phenobarbital. Three metabolites of phenobarbital.
22. Ewart, G. D., and Howells, A. J. ABC transporters involved in transport of eye pigment precursors in Drosophila melanogaster. In: S. Ambudkar and M. M. Gottesman eds. ; , Methods in Enzymology, Vol. 292, pp. 213224. San Diego, CA: Academic Press, Inc., 1998. 23. Honjo, Y., Hrycyna, C. A., Robey, R. W., Medina-Perez, W. Y., Yan, Q-W., van de Laar, A., Litman, T., Dean, M., and Bates, S. E. Acquired mutations in the MXR BCRP ABCP gene alter substrate specificity in MXR BCRP ABCP-overexpressing cells. Cancer Res., 61: 6635 6639, Kage, K., Tsukahara, S., Sugiyama, T., Asada, S., Ishikawa, E., Tsuruo, T., and Sugimoto, Y. Dominant-negative inhibition of breast cancer resistance protein as drug efflux pump through the inhibition of S-S homodimerization. Int. J. Cancer, 97: 626 630, Mickley, L., Jain, P., Miyake, K., Schriml, L. M., Rao, K., Fojo, T., Bates, S., and Dean, M. An ATP-binding cassette gene ABCG3 ; closely related to the multidrug resistance transporter ABCG2 MXR ABCP ; has an unusual ATP-binding domain. Mamm. Genome, 12: 86 88, Scheffer, G. L., Maliepaard, M., Pijnenborg, A. C. L. M., van Gastelen, M. A., de Jong, M. C., Schroeijers, A. B., van der Kolk, D. M., Allen, J. D., Ross, D. D., van der Valk, P., Dalton, W. S., Schellens, J. H. M., and Scheper, R. J. Breast cancer resistance protein is localized at the plasma membrane in mitoxantrone- and topotecan-resistant cell lines. Cancer Res., 60: 2589 2593, Rocchi, E., Khodjakov, A., Volk, E. L., Yang, C-H., Litman, T., Bates, S. E., and Schneider, E. The product of the ABC half-transporter gene ABCG2 BCRP MXR ABCP ; is expressed in the plasma membrane. Biochem. Biophys. Res. Comm., 271: 42 46, Maliepaard, M., Scheffer, G. L., Faneyte, I. F., van Gastelen, M. A., Pijnenborg, A. C. L. M., Schinkel, A. H., van de Vijver, M. J., Scheper, R. J., and Schellens, J. H. M. Subcellular localization and distribution of the breast cancer resistance protein in normal human tissues. Cancer Res., 61: 3458 3464, Jonker, J. W., Smit, J. W., Brinkhuis, R. F., Maliepaard, M., Beijnen, J. H., Schellens, J. H. M., and Schinkel, A. H. Role of breast cancer resistance protein in the bioavailability and fetal penetration of topotecan. J. Natl. Cancer Inst., 92: 16511656, 2000. Litman, T., Brangi, M., Hudson, E., Fetsch, P., Abati, A., Ross, D. D., Miyake, K., Resau, J. H., and Bates, S. E. The multidrug-resistant phenotype associated with overexpression of the new ABC half-transporter, MXR ABCG2 ; . J. Cell Sci., 113: 20112021, 2000. Ross, D. D., Yang, W., Abruzzo, L. V., Dalton, W. S., Schneider, E., Lage, H., Dietel, M., Greenberger, L., Cole, S. P. C., and Doyle, L. A. Atypical multidrug resistance: breast cancer resistance protein messenger RNA expression in mitoxantrone-selected cell lines. J. Natl. Cancer Inst., 91: 429 433, Maliepaard, M., van Gastelen, M. A., de Jong, L. A., Pluim, D., van Waardenburg, R. C. A. M., Ruevekamp-Helmers, M. C., Floot, B. J. G., and Schellens, J. H. M. Overexpression of the BCRP MXR ABCP gene in a topotecan-selected ovarian tumor cell line. Cancer Res., 59: 4559 4563, Kawabata, S., Oka, M., Shiozawa, K., Tsukamoto, K., Nakatomi, K., Soda, H., Fukuda, M., Ikegami, Y., Sugahara, K., Yamada, Y., Kamihira, S., Doyle, L. A., Ross, D. D., and Kohno, S. Breast cancer resistance protein directly confers SN-38 resistance of lung cancer cells. Biochem. Biophys. Res. Comm., 280: 1216 1223, Robey, R. W., Medina-Perez, W. Y, Nishiyama, K., Lahusen, T., Miyake, K., Litman, T., Senderowicz, A. M., Ross, D. D., and Bates, S. E. Overexpression of the ATP-binding cassette half-transporter, ABCG2 MXR BCRP ABCP1 ; , in flavopiridol-resistant human breast cancer cells. Clin. Cancer Res., 7: 145152, 2001. Komatani, H., Kotani, H., Hara, Y., Nakagawa, R., Matsumoto, M., Arakawa, H., and Nishimura, S. Identification of breast cancer resistance protein mitoxantrone resistance placenta-specific, ATP-binding cassette transporter as a transporter of NB-506 and J-107088, topoisomerase I inhibitors with an indolocarbazole structure. Cancer Res., 61: 28272832, 2001. Hazlehurst, L. A., Foley, N. E., Gleason-Guzman, M. C., Hacker, M. P., Cress, A. E., Greenberger, L. M., De Jong, M. C., and Dalton, W. S.
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With femur fracture. She reported a history of hypertension and valve abnormality. She admitted to worsening dyspnea over the past several months but had not yet seen her doctor about it. She denied chest pain. Her medications were lisinopril and hydrochlorothiazide. On admission, her blood pressure was 116 68 mm Hg, heart rate was 92 bpm, and Hgb Hct was 10.3 29.4 and stable. On exam, her lungs were clear, rhythm was regular with normal S1 and S2 and SEM 2 6, and she had 1 + edema in both legs. Her electrocardiogram revealed sinus rhythm with left bundle branch block and left ventricular hypertrophy. She was scheduled for urgent surgery for repair of the femur fracture. In the operating room, she was agitated and was given midazolam 2 mg prior to arterial line placement. After the midazolam the patient became combative, and reversal with.
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FISCAL YEAR 10-01-2004 CONFLICT MESSAGES 158 19, 653 CLAIMS PAID 151 19, 182 0 2 010 0 6, 409 0 10 1 7, PAID PCT 95.5 97.6 92.4 0.0 96.4 96.3 84.0 0.0 0.0 94.6 94.9 93.9 0.0 93.2 0.0 0.0 0.0 91.6 87.8 90.0 0.0 77.7 66.6 95.5 0.0 91.5 91.4 90.8 0.0 86.0 9.5 93.8 to 09-30-2005 DENY PCT 4.4 2.3 7.5 0.0 3.5 3.6 15.9 0.0 0.0 5.3 5.0 6.0 0.0 6.7 0.0 0.0 0.0 8.3 12.1 9.9 0.0 22.2 33.3 4.4 0.0 8.4 8.5 9.1 0.0 13.9 90.4 6.1 CLAIMS OVERIDDEN 0 31 61 206 0 18 6 576 0 148 11, 411 0 258 1 2, 0 1, 786 180 OVR PCT 0.0 0.1 1.6 0.0 0.0 0.4 6.1 5.0 0.0 0.0 4.6 5.0 1.2 0.0 0.0 1.2 0.0 0.0 0.0 2.8 0.0 1.6 6.5 0.3 0.0 3.2 0.0 0.2 5.1 3.0 0.0 0.7 5.6 4.5 0.0 16.3 25.0 2.0 0.0 5.5 3.3 7.7 CLAIMS REVERSED 1 394 77 0 0 124 19 189 0 220 0 1 0 234 19 45 0 1, 341 6, 0 111 0 4, 433 213 CLAIMS SCREENED 5, 520 245, TOT PCT 2.8 8.0 13.5 0.0 0.1 10.2 1.9 0.0 0.4 3.7 19.9 0.0 35.3 1.8 42.5 0.0 15.6 6.9 2.8 CLAIMS DENIED 7 471 305 0 10 334 298 0 114 17 478 0 0 664 31 122 0 289 0 256 38 7.
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Treatment options for dementia are now available, and increasing numbers of individuals with cognitive disorders are being evaluated for intervention. Little effort is made to select patients who will benefit from the various treatments. Widespread use of medication places patients at risk for developing side effects, which is one reason to target patients likely to benefit from specific interventions. We have limited health care resources and a growing population of elderly individuals with dementia, so our current system of "hit or miss" intervention will become increasingly costly and inefficient. Selecting.
Proposed Sequence of Treatments in CML All patients with CML transformed accelerated, blastic ; phases and those with a syngeneic donor should be offered allogeneic BMT ifthey are candidates for the procedure age less than 50 to 55 years, available matched or one antigen mismatched related donor ; . Younger patients age cut-off defined by investigators according to their experience in different age subgroups ; would be offered related allogeneic BMT in early chronic phase when possible, because of the high disease-free survival rates and low morbidity and mortality in these age groups. For the remaining patients, an initial trial of IFN-acontaining regimen may be indicated. If patients achieve a significant response any cytogenetic response at 6 months, Ph-positive cells less than 50% to 65% at 12 months ; they will continue on therapy unless the response is lost. The others will be offered allogeneic BMT from related donors, or investigational treatments such as MUD allogeneic BMT, autologous BMT, or new agents homohamngtonine, others ; or combinations Fig 4 ; . Patients who achieve a complete durable cytogenetic response documented over a 6-month period should have an autologous marrow storage. In them, IFN-a therapy should be held for at least 1 month before autologous marrow preservation for ease of procedure and storage of an adequate and sirolimus.
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Running Title: P2X7 receptor-mediated glutamate release Address correspondence to: Giorgio Carmignoto, Istituto CNR di Neuroscienze and Dipartimento di Scienze Biomediche Sperimentali, Universit di Padova, viale G. Colombo 3, 35121 Padova, Italy, Tel. + 39 049 8276075; Fax. + 39 049 8276049; E-mail: gcarmi bio pd The purinergic P2X7 receptor P2X7R ; can mediate glutamate release from cultured astrocytes. Using patch-clamp recordings, we investigated whether P2X7Rs have the same action in hippocampal astrocytes in situ. We found that 2-& 3-O- 4-benzoylbenzoyl ; ATP BzATP ; , a potent, although unselective, P2X7R agonist, triggers two different, glutamate-mediated responses in CA1 pyramidal neurons: transient inward currents, that have the kinetical and pharmacological properties of previously described slow inward currents SICs ; due to Ca2 + -dependent glutamate release from astrocytes, and a sustained tonic current. While SICs were unaffected by P2X7Rs antagonists, the tonic current was inhibited, amplified in low extracellular Ca2 + and was insensitive to glutamate transporter and hemichannel inhibitors. BzATP triggered in astrocytes a large depolarization that was inhibited by P2X7R antagonists and amplified in low Ca2 + . In low Ca2 + , BzATP also induced lucifer yellow uptake into a subpopulation of astrocytes and CA3 neurons. Our results demonstrate that purinergic receptors other than the P2X7R mediate glutamate release that evokes SICs, while activation of a receptor that has features similar to the P2X7R, mediates a sustained glutamate efflux that generates a tonic current in CA1 neurons. This sustained glutamate efflux that is potentiated under non-physiological conditions, may have important pathological actions in the brain. INTRODUCTION Glutamate is the principal mediator of excitatory neurotransmission in the central nervous system as well as a recognized excitotoxic agent that can lead neurons and astrocytes to death when present at excessive extracellular concentrations 1, 2 ; . The ability to release this transmitter 3-5 ; hints at a direct participation of astrocytes in glutamatergic neuronal transmission as well as in the excitotoxic action of glutamate. While this latter issue remains to be proved, increasing evidence indicates that astrocyte-derived glutamate has complex actions on neurons exerting a modulatory role on synaptic transmission. For example, in the retina the release of glutamate from astrocytes modulates ganglion cell spike activity driven by light stimulation, most likely through a presynaptic action 6 ; . In the hippocampus, it modulates excitability of interneurons and potentiates inhibitory transmission 7, 8 it acts also on excitatory axon terminals of the CA1 region to increase the probability of spontaneous glutamate release 9 ; . At the same time, astrocytic glutamate exerts a direct action on hippocampal pyramidal neurons by activating extrasynaptic NMDARs and triggering episodic, inward currents characterized by slow kinetics SICs ; 10, 11 ; . Interestingly, this NMDAR response can occur synchronously in multiple CA1 neurons raising the possibility that it may serve to promote synchrony of neuronal activity 10, 11 ; . As to the mechanism of glutamate release, it is known that [Ca2 + ]i elevations in astrocytes can rapidly trigger the fusion with the plasma membrane of glutamate containing vesicles 12, 13 ; . While this exocytosis-mediated pathway is most likely involved in astrocyte-to-neuron signaling under physiological conditions, other mechanisms may contribute to this process under both physiological and pathological conditions 14, 15 ; . Recently, a glutamate release mechanism that involves the P2X7R has been proposed 16 ; . This receptor has an established role in cellular toxicity and inflammatory processes 17, 18 ; . Upon sustained activation with ATP it can form a pore permeable to molecules of relatively large size 900 Da ; thus allowing molecules, such as glutamate, to efflux from, or enter into, the.
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| Secobarbital pillsThe convertible notes mature on September 30, 2010, unless earlier converted or repurchased. In addition to its internal research and development costs, the Company, from time to time, enters into agreements with third parties with respect to the development of new products and technologies. To date, the Company has entered into agreements and advanced funds or has commitments with several non-affiliated companies for products in various stages of development. These types of payments or commitments are generally dependent on a third party achieving certain milestones or the timing of third party research and development or legal expenses. Due to the uncertainty of the timing or realization of such commitments, these obligations are not included in the table above; however, agreements that contain such commitments that the Company believes are material are described below. Payments made pursuant to these agreements are either capitalized or expensed according to the Company's accounting policies. Par and Nortec entered into an agreement, dated October 22, 2003, in which the two companies agreed to develop additional products that are not part of the two previous agreements between Par and Nortec. During the first two years of the agreement, Par is obligated to make aggregate initial research and development payments to Nortec in the amount of , 000, of which , 500 was paid by Par in fiscal year 2003, , 000 is due in fiscal year 2004 and 0 is due in fiscal year 2005. On or before October 15, 2005, Par has the option to either i ; terminate the arrangement with Nortec, in which case the initial research and development payments will be credited against any development costs that Par shall owe Nortec at that time or ii ; acquire all of the capital stock of Nortec over the subsequent two years, including the first fifty 50% ; percent of the capital stock of Nortec over 30 and solifenacin.
10 Inoue M, Kimura T, Ota K, Iitake K, Shoji M, Sato K, Ohta M & Yoshinaga K. Effect of vasopressin on atrial natriuretic peptide release and renal function in dogs. American Journal of Physiology 1988 255 E449E455. 11 Inoue M, Kimura T, Ota K, Shoji M, Sato K, Ohta M, Yamamoto T & Yoshinaga K. Effect of atrial natriuretic peptide on the vasopressin response to osmotic and hemorrhagic stimuli in dogs. Journal of Neuroendocrinology 1990 2 903909. Kimura T, Abe K, Ota K, Omata K, Shoji M, Kudo K, Matsui K, Inoue M, Yasujima M & Yoshinaga K. Effects of acute water load, hypertonic saline infusion, and furosemide administration on atrial natriuretic peptide and vasopressin release in humans. Journal of Clinical Endocrinology and Metabolism 1986 62 1003 Kimura T, Matsui K, Ota K & Yoshinaga K. Radioimmunoassay of arginine vasopressin in human plasma and urine, a resin microcolumn method. Tohoku Journal of Experimental Medicine 1980 131 3746. Ghani M, Vincent DS & Richard MS. Effects of chronic sodium depletion on tubular sodium and water reabsorption in the dog. American Journal of Physiology 1974 227 469476. Sampanta B, Jay HS, Richard B, Richard WO, Willa H, Stanley C, David Y & Thomas FF. Effect of plasma sodium concentration on diluting segment sodium reabsorption. Kidney International 1974 5 111. Wang BC, Share L, Crofton JT & Kimura T. Effect of intravenous and intracerebroventricular infusion of hypertonic solutions on plasma and cerebrospinal fluid vasopressin concentrations. Neuroendocrinology 1982 34 215221. Ota K, Kimura T, Matsui K, Iitake K, Shoji M, Inoue M, Sato K, Ohta M, Yamamoto T & Yoshinaga K. Effects of central osmotic stimulation on vasopressin and enkephalin release into the blood and cerebrospinal fluid and blood pressure. Acta Endocrinologica 1990 122 6270.
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Previous studies have shown that microtubules were distributed in ameloblasts, odontoblasts and periodontal fibroblasts. The purpose of this study was to describe in more detail the distribution of microtubules in these cells of the rat maxillary incisor. Rats were perfused with 10 % formalin. Their maxillae were removed, demineralized in 7 5 EDTA, dehydrated and embedded in paraffin. Sagittal sections were cut at 5 cm and then incubated with af finity purif ied rabbit anti-tubulin antibody, followed by fluorescein-conjugated goat anti-rabbit IgGs. In the secretary ameloblasts, immunofluorescence labelling for tubulin was observed in the cytoplasm and Tomes' process. An intense fluorescence was seen in the young and old odontoblastic cell bodies. In the labial dentinal and somatropin
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