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The CFU colony forming units ; of the samples from 31 root canals from deciduous teeth with necrotic pulp and radiographically visible periapical lesion are presented in Table 1. The prevalence of anaerobic microorganisms was 96.8% 30 root canals ; , and black-pigmented bacillus BPB ; were found in 11 cases 35.5% ; . Aerobic microorganisms were present in 29 root canals 93.5% ; with streptococci present in 30 canals 96.8% ; . Streptococcus mutans was quantified in 15 canals 48.4% ; whereas Streptococcus sobrinus was not detected.
Studieson synaptosomes from severalbrain regionshave shown that nicotine could activate the releaseof neurotransmitter in a TTX-independent manner seeWonnacott et al., 1990, for review ; , thus suggesting direct link between nAChR activation a and cytosolic calcium elevation associated with the transmitter releaseprocess.In contrast, the presynaptic action of nicotine that we have described in the IPN was blocked by TTX. This effect could be attributed to an activation of nAChRs located on the somatodendritic region of intrinsic neurons, and subsequenttriggering of action potentials. However, we show that the presynaptic action of nicotine observed in IPN thin slices can be reproduced usinga preparation of isolated neuronsthat had retained synaptic contacts. In this preparation, neuronsare physically isolated from one another, in such a way that the synaptic activity that we recorded could only be attributed to the activation of terminal axonal afferents attached to the cell body. In this preparation, the increase in PSC frequency by nicotinic agonistswasalso blocked by TTX, indicating that the nAChRs involved are different in their location from the presynaptic nAChRs described synaptosomal in preparations.These experimentsthus suggest presence "preterminal" nAChRs, the of located on terminal regionsof the axon but not in the proximity of a singlesynaptic bouton. Our data suggest that activation of thesenAChRs directly triggersTTX-sensitive spikesin the terminal portion of the GABAergic axons. Theseaction potentials presumably initiate synchronous GABA releasefrom multiple presynaptic terminals. We do not exclude that part of the effect of nicotinic agonists observed in thin slicescould be due to the activation of postsynaptic nAChRs located on the soma or dendrites of intrinsic IPN neurons. However, nicotinic agonistsshow a presynaptic action at concentrations roughly 10 times lower than thosenecessaryto activate a postsynapticresponse theseIPN neurons. in This finding suggests that preterminal and somatic nAChRs might be different subtypesof nAChRs, and that at low micromolar concentrations of agonist, only the preterminal nAChRs are activated. The order of potency of nicotinic agonistsfor the preterminal action is in the order cytisine nicotine ACh in the presenceof eserine ; DMPP. However, cytisine is about threefold more potent than DMPP. In contrast, for postsynaptic nAChRs, cytisine is about 30 times more potent than DMPP Mulle et al., 1991 ; . Thus, these findings would be in favor of the hypothesisthat the postsynaptic and the preterminal actions are not mediated by the same subtype of nAChR. However, this remainsto be firmly establishedby, for instance, the useof subunit-specificantibodies. How do thesepreterminal nAChRs affect the function of synaptic circuits in the IPN? A large population of glutamic acid decarboxylase GAD ; -containing neuronalcell bodieshave been describedin the IPN Kawaja et al., 1989 ; and most, if not all, GABAergic afferents arise from these intrinsic neurons. It is thus most likely that the preterminal nAChRs are not located on fasciculusretroflexus fibers, although thesefibers have been shown to possess presynaptic nAChRs in various anatomical and physiological studies Brown, 1984; Clarke et al., 1986; Mulle et al., 1991 ; . GABAergic neurons in the IPN are likely to expressthe preterminal nAChRs on their local axon terminals. We do not know whether these GABAergic neurons also possess postsynaptic nAChRs found on acutely isolated neuthe rons and in the thin-slice preparation. However, this seems unlikely since the regions from which most recordings were made do not coincide with the regionsof high density of GAD.
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Although genomic instability is a hallmark of human cancer cells, the mechanisms by which genomic instability is generated and selected for during oncogenesis remain obscure. In most human cancers, the pathway leading to the activation of the G1 cyclins is deregulated. Using budding yeast as a model, we show that overexpression of the G1 cyclin Cln2 inhibits the assembly of prereplicative complexes pre-RCs ; and induces gross chromosome rearrangements GCR ; . Our results suggest that deregulation of G1 cyclins, selected for in oncogenesis because it confers clonal growth advantage, may also provide an important mechanism for generating genomic instability by inhibiting replication licensing. [Keywords: G1 cyclin; genomic instability; prereplicative complex; DNA replication; cell cycle control; oncogenesis].
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We thank Russell Jones for AICAR. S.B.K. was supported by NIH training grant T32-AI-07324 awarded by NIAID. This work was supported by the National Institutes of Health through Public Health Service grant CA28379 awarded to J.C.A. by the National Cancer Institute and frovatriptan.
An agent 8-OH-DPAT, a selective agonist of the 5-HT1A subtype of serotonin receptors, protects cells against an excitotoxic effect of NMDA181 and stimulates an increase of extracellular acetylcholine in the brain in experimental animal models ; .182.
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Situation through PRA techniques and formed village health committees. Community volunteers have been selected from each village by the village health committees, these volunteers are envisaged as the health spokespersons of the villages. Block wise training programs have been conducted from 19th to 24th December 2006 to train the volunteers on their role and responsibilities for community health. Information on public health facilities and schemes has been provided to the volunteers by the medical officers of the concerned block PHCs. The other domains of the training like community health, importance of community participation in health activities, assessing community health situation, community health planning, etc. were dealt by Mr. Ranjan Kumar Raul, SDO, BOLEP and Mr. P.K. Mishra, PO. A total of 127 including 36 female volunteers attended the program and fulvestrant.
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New ; Environment 18 Calls on all States to ensure the health and well- being of children by WFC ; managing natural resources, protecting and conserving the environment in a sustainable manner WFC NGO text ; , re- examining and revising industrial, commercial and development priorities and processes with a strong and effective imperative of preserving and regenerating the bio - diverse environment, and rapidly reducing and reversing environmental damage, WFC ; to work to change unsustainable patterns of production and consumption . Freedom from violence 19. new ; Reaffirms paragraphs 17-21 of its resolution 2002 92 and the vital importance of the Study on Violence Against Children in gaining significant international attention to this issue and ways of eliminating such violence, in accordance with the Convention on the Rights of the Child, 20. new ; Welcomes the collaboration of the Office of the High Commissioner for Human Rights, the World Health Organisation and the United Nations Children's Fund in supporting the independent expert and calls on him to ensure the meaningful participation of children -the inclusion of their experiences and perspectives-, NGOs, academic institutions, governments, UN, regional and other relevant bodies in the preparation for the study and its follow- up. 21. new ; Recalls the importance for the study of the recommendations of the two theme days of the Committee on the Rights of the Child and calls on the independent expert to collaborate closely with the Committee on the Rights of the Child in the course of the study 21bis Urges member States to support the study with financial contributions and to support national- level research and collaboration by NGOs.
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Management reaffirmed top and bottom line guidance for 2006, and as such, we are maintaining our 2006 eps estimate of $ 7 endo's business continues to advance, with a potential oxymorphone product approval in june, an snda filing for frova in menstrual migraines expected in june, and rapinyl and ketoprofen patch in and entering phase 3 studies, respectively.
The 5-year relative survival10 for stomach cancer was estimated to increase in Italy from 12% for male patients diagnosed in the period 1978-1982 to 23% for those diagnosed in the period 1992-1994, and from 17% to 29% for women during the same periods of diagnosis. The estimated proportion of cured patients was on average 22% for both sexes for the entire period of diagnosis 19781994, and the mean survival time for those who were not cured was on average 18 months. Survival was higher in northern and central regions than in southern regions. Detailed results on stomach cancer survival analysis are reported in a technical document available from the project website. Figure 1 reports age-standardized mortality and incidence trends in Italy. Incidence and mortality trends were estimated to be clearly decreasing during the period 1970-2010. The yearly incidence rate is estimated to decrease by 59% in men from 46 to 19 per 100, 000 ; and by 65% in women from 24 to 8 per 100, 000 ; . The de and gabitril.
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References: Diener HC et al. J Neurol Sci 1996; 143: 1-13. Sixth ACCP Consensus Conference on Antithrombotic Therapy. Albers G et al. Chest 2001; 119 Suppl 1 ; : 300s-320s. EUSI Recommendations for Stroke Management, Update 2003. Cerebrovasc Dis 2003; 16: 311-37. Eisert WG. Platelets. Academic Press, pp. 803-815, 2003. Serebruany V. J Hematol 2004; 75: 40-47.
Results include Record Quarterly and Nine-Months Net Sales CHADDS FORD, Pa., Nov. 1, 2007 -- Endo Pharmaceuticals Holdings Inc. Nasdaq: ENDP ; , a specialty pharmaceutical company with market leadership in pain management, today reported financial results for the three months and nine months ended September 30, 2007. Net sales for the third quarter of 2007 grew by 24% to a record 9.5 million compared with 7.1 million in the third quarter of 2006. Net income for the three months ended September 30, 2007 was .1 million compared with .9 million in the same period of 2006. As detailed in the Supplemental Financial Information below, adjusted net income for the three months ended September 30, 2007 was .6 million compared with .2 million in the same period in 2006. Diluted earnings per share for the three months ended September 30, 2007 were ##TEXT##.44 compared with ##TEXT##.33 in the comparable 2006 period. As detailed in the Supplemental Financial Information below, adjusted diluted earnings per share for the three months ended September 30, 2007 were ##TEXT##.46 compared with ##TEXT##.35 in the same period in 2006, an increase of 31%. "This excellent quarterly performance is indicative of the strength of our business, " said Peter A. Lankau, President and Chief Executive Officer. "Underlying demand remains strong for LIDODERM, the OPANA franchise, and FROVA, and we continue to implement key initiatives aimed at delivering long-term shareholder value." Lankau also noted that, consistent with its goal of becoming the leading pain company, Endo is continuing to focus its business development activities on product licensing and acquisitions to deepen its penetration in pain management while seeking to diversify its revenue base in the near-term through company acquisitions in selected specialty-focused therapeutic areas. Revised EPS Guidance Based primarily on lower-than-expected SG&A costs associated with pre-launch marketing and promotional initiatives for FROVA following the disclosure on September 30, 2007 that the U.S. Food and Drug Administration had issued a "not approvable" letter in response to Endo's supplemental New Drug Application sNDA ; for FROVA for the short-term prevention of menstrual migraine, the company is increasing its earnings per share guidance for 2007. The company estimates adjusted diluted earnings per share excluding estimated milestone payments to partners and the expensing of stock-based compensation charges ; for 2007 to be approximately .79 to .84, up from the prior adjusted diluted EPS guidance of .75 to .80. Endo also reiterated its 2007 net sales guidance of approximately .050 billion to .075 billion, which includes estimated net sales of LIDODERM of approximately 5 million to 0 million and estimated combined net sales of the OPANA franchise of approximately million to 0 million and garlic.
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18. Jeffery D, Arnason B, Bigley G, Coyle P Goodin D, Hurwitz B et al., "MRI outcomes in relapsing-remitting multiple sclerosis , patients treated with 500 mcg INFB-1b versus 250 mcg every other day: first phase of the BEYOND programme", Multiple Sclerosis 2004 10 2 ; : S244. 19. Berger J R, Koralnik I J, "Progressive Multifocal Leukoencephalopathy and Natalizumab-Unforeseen Consequences", N. Engl. J. Med. 9 June 2005 ; E-pub ahead of print and frova.
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The New York Time, Carlotta Gall, `Afghan Poppy Farmers Say Mystery Spraying Killed Crops, 5 December 2004 The New York Times, Thom Shanker, `Pentagon Sees Antidrug Effort in Afghanistan' 25 March 2005, p.1 The Sun Newspaper, `Operation opium: 2, 500 of our boys take on Afghan warlords', 22 August 2005 The Times, Catherine Philip, `Britain blamed as opium farms harvest bumper crop', 23 May 2005 Tony Addision, Does the Global Economy Work for Peace?, Discussion Paper No. 2005 05, United Nations University, World Institute for Development Economics Research, February 2005 UN, The Single Convention on Narcotic Drugs of 1961, as amended by the 1972 Protocol UNDP, Afghanistan Staff Newsletter, June 2005. : undp .af media room news letter docs news letter 20050601.p df UNODC, The Opium Situation in Afghanistan, 29 August 2005 UNODC. Afghanistan Opium Survey 2004. November 2004 Vanda Felbab-Brown, Afghanistan: When Counternarcotics Undermines Counterterrorism, The Washington Quarterly, The Centre for Strategic and International Studies and the Massachusetts Institute of Technology, Autumn 2005, pp. 55-72 WHO Special Report, Central Asia Crisis Unit, 29 October 2001 WHO, Cholera in Afghanistan, Communicable Disease Surveillance & Response, 21 June 2005 : who.int csr don 2005 06 21 en index WHO, Diphtheria in Afghanistan, Communicable Disease Surveillance & Response, 29 August 2003 : who.int csr don 2003 08 29 en index World Bank. Afghanistan: State Building, Sustaining Growth, and Reducing Poverty. A Country Economic Report, Poverty Reduction and Economic Management Sector Unit South Asia Region, World Bank Report No 29551 AF, 2004 and frovatriptan.
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1. Rantuccio F, Mastrolonardo M, Conte A. Area Celsi. Osservazioni personali e revisione della letteratura. G Ital Dermatol Venereol. 1995; 130: 23-35. Dawber R. Alopecia areata. Monogr Dermatol. 1989; 2: 89-102. Moreno GA, Ferrando J. Alopecia areata. Med Cutan Ibero Latina Americana. 2000; 28: 294-312. Dawber RPR, de Berker D, Wojnarowska F. Disorders of hair. In: Champion RH, Burton JL, Burns DA, Breathnach SM, editors. Textbook of dermatology. Oxford: Blackwell Science; 1998. p. 2919-27. Ferrando Roqueta FJ, Corral Blanco C, Lobo Satue A, Grasa Jordan MP Estudios clnicos y de laboratorios Estudio de los fenmenos de estrs y su relacin con variables psicopatolgicas, clnicas e imunolgicas en pacientes com alopacia areata. Actas Dermatosifiliogr. 1996; 87: 597-609. Price V. Alopecia areata: clinical aspects. J Invest Dermatol. 1991; 96: 685. Camacho F. Alopecia areata: clinical features. Dermatopathology. In: Camacho F, Montagna W, editors. Trichology: diseases of the pilosebaceus follicle. Madrid: Aula Medica Group; 1997. p.417-40. Pimentel ERA. Alopecia areata. Aspectos imunolgicos e tratamento pelo DNCB. [Tese]. Universidade de So Paulo; 1988. Safavi K. Prevalence of alopecia areata in the First National Health and Nutrition Examination Survey letter ; . Arch Dermatol. 1992; 128: 702. Safavi KH, Muller SA, Suman VJ, Moshell AN, Melton LJ. Incidence of alopecia areata in Olmsted County, Minnesota, 1975 through 1989. Mayo Clin Proc. 1995; 70: 628-33. Shapiro J, Modani S. Alopecia areata: diagnosis and management. Int J Dermatol. 1999; 38: 19-24. Tosti A, Fanti PA, Morelli R, Bardazzi F. Trachyonichia associated with alopecia areata: a clinical and pathological study. J Acad Dermatol. 1991; 25: 266-70. Bergner T, Donhauser G, Ruzicka T. Red lunula in severe alopecia areata. Acta Dermato Venereol Stockh ; . 1992; 72: 203-5. Tosti A, Morelli R, Bardazzi F, Peluso AM. Prevalence of nail abnormalities in children with alopecia areata. Pediatr Dermatol. 1994; 11: 112-5. Sahn EE. Alopecia areata in childhood. Semin Dermatol. 1995; 14: 9-14. Tosti A, Colombati S, De Padova MP Guidi SG, Tosti G 17. Maccolini E. Retinal pigment epithelium function in AA. J Invest Dermatol. 1986; 86: 553-5. Tosti A, Colombati S, Caponeri GM, Ciliberti C, Tosti G, Basi M, et al. Ocular abnormalities occurring with alopecia areata. Dermatologica. 1985; 170: 69-73. Muller SA, Brunsting LA. Cataracts associated with dermatologic disorders. Arch Dermatol. 1963; 88: 330-9. Hordinsky MA. Alopecia areata. In: Olsen EA, editor. Disorders of hair growth. Diagnosis and treatment. New York: MacGraw-Hill, 1994. p.195-222. Ikeda T. Produced alopecia areata based on the focal infection theory and mental theory. Dermatologica. 1967; 134: 1-11. Hatzis J, Kostakis P Tosca A, Parissis N, Nicolis G Varelzidis A, et al. Nuchal nevus flammeus as a skin marker of prognosis in alopecia areata. Dermatologica. 1988; 177: 149-51. Camacho F, Navas J. Nuchal nevus flammeus and alopecia areata. Dermatology 1992; 184: 58. Muller SA, Winkelmann RK. Alopecia areata: an evaluation of 736 patients. Arch Dermatol. 1963; 88: 290-7. Shellow WV Edwards JE, Koo JY. Profile of alopecia , areata: a questionnaire analysis of patient and family. Int J Dermatol. 1992; 31: 186-9. Scerri L, Pace JL. Identical twins with identical alopecia areata. J Acad Dermatol. 1992; 27: 766-7. Jackow C, Puffer N, Hordinsky M, Nelson J, Tarrand J, Duvic M. Alopecia areata and cytomegalovirus infection in twins: genes versus environment? J Acad Dermatol. 1998; 38: 418-25. Weidmann Al, Zion LS, Mamelok AE. Alopecia areata occurring simultaneously in identical twins. Arch Dermatol. 1956; 74: 424-32. Du Vivier A, Munro DD. Alopecia areata, autoimmunity and Down's syndrome. Br Med J. 1975; 1: 191-4. Colombe BW Price VH, Khoury EL. HLA class II antigen , associations help to define two types of alopecia areata. J Acad Dermatol. 1995; 33: 757-64. Frentz G, Thomsen K, Jakobsen BK, Svejgaard. HLADR4 in alopecia areata [letter]. J Acad Dermatol. 1986; 13: 129-30. Mikesell JF, Bergfeld WL, Braun WE. HLA-DR antigens in alopecia areata: preliminary report. Cleve Clin Q. 1986; 53: 189-91. Orecchia G, Belvedere MC, Martinetti M. Human.
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