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Several rice cultivars have demonstrated allelopathic property against barnyardgrass or other weeds. Among the rice cultivars evaluated from prior screening procedures to distinguish between competition and allelopathy, field experiments, and greenhouse studies, TN1 had shown allelopathic effect against barnyardgrass, horsepurslane Trianthema portulacastrum L. ; , ducksalad Heteranthera limosa ; , and Ammannia sp. Dilday et al., 1998; Olofsdotter et al., 1997 ; . Cultivar TN1 was chosen for extraction and isolation of allelochemicals, not only for being the "parent" allelopathic cultivar but also because of results obtained from preliminary studies. In a blinded study, root extracts from three rice samples V69, V216, and VO1 ; were tested for activity against lettuce and barnyardgrass using 24-well culture plate assay. Sample V01, which was an extract of TN1, inhibited the growth of barnyardgrass significantly Table 1 ; . The TN1 cultivar also carries the gene for semiTable 1. Effect of rice root extracts on lettuce and barnyardgrass, for example, ditropan work.
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1. NCRP Development of an Atlas of Cancer in India, 2001-2002. Volume I. National Cancer Registry Programme Indian Council of Medical Research ; , Bangalore [ canceratlasindia ], 2004a 2. NCRP Development of an Atlas of Cancer in India, 2001-2002. Volume II National Cancer Registry Programme Indian Council of Medical Research ; , Bangalore [ canceratlasindia ], 2004b 3. Nandakumar A., Gupta PC, Gangadharan P., Visweswara RN and Parkin DM: Geographic Pathology Re-visited Development of an Atlas of Cancer in India, Int J Cancer under Publication, for example, ditropan use.
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Study, increased serum CA 15-3 predicted worsened survival in both univariate and multivariate models Table 5 ; . Increased serum HER-2 neu also predicted a worsened prognosis. The interaction of the two markers with regard to effect on survival is shown in Fig. 3. Increased serum CA 15-3 alone was associated with a poorer prognosis than when neither marker was increased. Patients with increased serum HER-2 neu and serum CA 15-3 had a shorter survival than did patients with an increased serum CA 15-3 alone and
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Background: Altering norms may be an important means to introduce and sustain health protective behavior change. The paper argues that i ; normative considerations are more important than attitudinal factors in promoting CRC screening adherence, and ii ; the concept of subjective norm should be treated as a multi-layered construct which involves several key contextual characteristics. Methods: Structural equation modeling was used to evaluate components within the theories of reasoned action TRA ; , planned behavior TPB ; , and social cognitive theory SCT ; for understanding CRC screening adherence in a population-based community sample of 341 Japanese Americans aged 50 and over residing in the Greater New York region. Results: The data fit a mediational model P 127 ; 209.7, GFI 0.94, CFI 0.97, RMSEA 0.04 ; . The model accounted for 47% of the variance in CRC screening adherence. Among key cognitive variables family friend-norms, providernorms, perceived behavioral control, and perceived benefits ; , CRC screening adherence was most strongly associated with family friend norms regarding CRC screening use. Family emotional support, but not the size of the networks, was most positively related to family friend-norms. While having usual source of care was positively and directly associated with screening adherence, better physician-patient relationships positively and indirectly associated with screening adherence via increased perceived benefits. Conclusions: The findings of this study may have implications for norm change interventions via family networks among older Japanese American communities at high risk for CRC. CORRESPONDING AUTHOR: Keiko Honda, Ph.D., MPH, Epidemiology, Columbia University, 722 West 168th St., Rm 719, New York, NY, USA, 10032; kh2086 columbia and
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In authorizing DCH to propose changes in the Medicaid pharmacy benefit, Michigan legislators assumed the new program would produce savings of nearly $43 million in state fiscal year 2002. The $43 million was subtracted from the Medicaid appropriation for the year.37 To achieve the full savings, DCH proposed an aggressive timetable to implement the MPPL quickly. Implementation, however, was interrupted several times due to the legislative approval process outlined in PA 60 and the litigation against the MPPL. In its initial plan for the MPPL sent to the legislature on September 28, 2001 ; , DCH set the program launch date on December 1, 2001. Approval of the plan by the legislature was delayed until November 14, 2001 when the House Speaker and Senate Majority Leader sent the letter of understanding to DCH ; . DCH established a second implementation date of January 14, 2002. PhRMA filed suit in Michigan circuit court over the MPPL on November 30, 2001 described below in Section V ; . The state delayed the projected implementation until February 1, 2002 and pseudoephedrine and ditropan, for instance, dittopan mechanism of action.
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Hypothesis: Small-bowel diaphragm disease is an important source of gastrointestinal tract bleeding and subacute intestinal obstruction that may require surgical intervention. Design: Case series. Setting: Tertiary-care academic medical center. Patients: Seven consecutive patients with histologi, because robinol dirtopan and propanthelin!
7. Blachy P, Gowing D. Multiple monitored electroconvulsive treatment. Compr Psychiatry 1966; 7: 100109. Figiel GS, McDonald WM, McCall WV, et al. Electroconvul sive therapy. In: Schatzberg AF, Nemeroff CB, eds. Textbook of psychopharmacology. Washington, DC: American Psychiatric Press, 1995: 523543. 9. Abrams R. The mortality rate with ECT. Convuls Ther 1997; 13 3 ; : 125127. 10. Salzman C. ECT, research, and professional ambivalence [edito rial] [see comments]. J Psychiatry 1998; 155 1 ; : 12. 11. Rudorfer MV, Goodwin FK. Introduction. In: Coffey CE, ed. The clinical science of electroconvulsive therapy, vol. 38. Washington, DC: American Psychiatric Press, 1993: xviixxi. 12. Ottosson J-O. Experimental studies of the mode of action of electroconvulsive therapy. Acta Psychiatr Neurol Scand 1960; 35: 1141. Fink M, Johnson L. Monitoring the duration of electroconvul sive therapy seizures: `cuff' and EEG methods compared. Arch Gen Psychiatry 1982; 39 10 ; : 11891191. 14. Maletzky BM. Seizure duration and clinical effect in electrocon vulsive therapy. Comp Psychiatry 1978; 19 6 ; : 541550. 15. Abrams R, Taylor MA. Diencephalic stimulation and the effects of ECT in endogenous depression. Br J Psychiatry 1976; 129: 482485. Fink M, Ottosson JO. A theory of convulsive therapy in endoge nous depression: significance of hypothalamic functions. Psy chiatry Res 1980; 2 1 ; : 4961. 17. Mathe AA. Neuropeptides and electroconvulsive treatment. J Ect 1999; 15 1 ; : 6075. 18. Sackeim HA, Decina P, Kanzler M, et al. Effects of electrode placement on the efficacy of titrated, low-dose ECT. J Psy chiatry 1987; 144 11 ; : 14491455. 19. Devanand DP, Lisanby S, Lo ES, et al. Effects of electroconvul sive therapy on plasma vasopressin and oxytocin. Biol Psychiatry 1998; 44 7 ; : 610616. 20. Lisanby SH, Devanand DP, Prudic J, et al. Prolactin response to electroconvulsive therapy: effects of electrode placement and stimulus dosage [see comments]. Biol Psychiatry 1998; 43 2 ; : 146155. 21. Krystal AD, Weiner RD, McCall WV, et al. The effects of ECT stimulus dose and electrode placement on the ictal electroen cephalogram: an intraindividual crossover study. Biol Psychiatry 1993; 34 11 ; : 759767. 22. Nobler MS, Sackeim HA, Solomou M, et al. EEG manifesta tions during ECT: effects of electrode placement and stimulus intensity. Biol Psychiatry 1993; 34 5 ; : 321330. 23. Weiner RD, Krystal AD. EEG monitoring of ECT seizures. In: Coffey CE, ed. The clinical science of electroconvulsive therapy, vol. 38. Washington, DC: American Psychiatric Press, 1993: 93109. 24. Krystal AD. The clinical utility of ictal EEG seizure adequacy models. Psychiatric Ann 1998; 28 1 ; : 3035. 25. Krystal AD, Zaidman C, Greenside HS, et al. The largest Lyapu nov exponent of the EEG during ECT seizures as a measure of ECT seizure adequacy. Electroencephalogr Clin Neurophysiol 1997; 103 6 ; : 599606. 26. Krystal AD, Coffey CE, Weiner RD, et al. Changes in seizure threshold over the course of electroconvulsive therapy affect therapeutic response and are detected by ictal EEG ratings. J Neuropsychiatr Clin Neurosci 1998; 10 2 ; : 178186. 27. Krystal AD, Weiner RD, Coffey CE. The ictal EEG as a marker of adequate stimulus intensity with unilateral ECT. J Neuro psychiatr Clin Neurosci 1995; 7 3 ; : 295303. 28. McCall WV, Farah A, Reboussin D. Can we teach psychiatric residents to rate seizure regularity? Convuls Ther 1995; 4: 248252 and
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368 DIFFERENTIAL SUPPRESSION OF DENGUE VIRUS REPLICATION BY NITRIC OXIDE. Ubol S, Takumpanya R, Mammen PM, Endy PT, Libraty D. Department of Microbiology, Mahidol University, Bangkok, Thailand; Division of Virology, Armed Force Research Institute of Medical Science, Bangkok, Thailand; Department of Medicine and Infectious Diseases, CIDVR, University of Massachusetts School of Medicine. Dengue virus DV ; is a member of an arthropod-born Flavivirus which affects up to 100 million individuals annually. It causes a spectrum of diseases ranging from asymptomatic infection, mild illness to severe disease with fatal. DV actively replicates in various types of immune cells especially the one that is well accepted as professional nitric oxide producer, monocyte macrophage and dendritic cell. The interaction between nitric oxide NO ; and DV in these target cells is unknown. Therefore, we performed an experiment to investigate the effect of NO on vitro replication of 26 isolates of DV. These viruses are primarily isolates from DF and DHF patients 13 DF and 13 DHF ; . N18 cells were infected with either DF or DHF isolate and immediately treated with 50 or 75 SNAP, an exogenous NO donor. Production of viral progenies in the present and absent of NO was followed by monitoring the copy number of genomic viral RNA using TaqMan RT-PCR. It was found that NO exerted an inhibitory effect on DV replication. SNAP at 75 M generated NO high enough to suppress all 26 isolates. However, at lower concentration of NO, 50uM SNAP, the susceptibility of DF and DHF isolates to inhibitory effect of NO was difference. We found that 77% of DF isolates were susceptible while only 54% of DHF isolates were affected. In conclusion, NO negatively regulates DV replication. The degree of suppression is dependent on phenotype of virus.
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