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FIRST HORIZON PHARMACEUTICAL CORPORATION NOTES TO CONSOLIDATED FINANCIAL STATEMENTS -- CONTINUED ; provisions in the event of a change in control, as defined in the plan. In 2000, the Company terminated the 1997 Plan and no additional grants of stock options will be made under the 1997 Plan. At December 31, 2001, 1, options remained issued and outstanding under the 1997 Plan. On February 14, 2000, the Board of Directors and stockholders approved the 2000 Stock Plan the "2000 Plan" ; . This plan provides for the granting of incentive stock options, nonqualified stock options, stock awards or stock bonuses, and sales of stock. The 2000 Plan provides for the grants of these options and other awards to officers, directors, full- and part-time employees, advisors and consultants. Only full-time employees may receive incentive stock options. The Company has reserved 3, 000, 000 shares of common stock for issuance under the 2000 Plan. The Company's compensation committee administers the 2000 Plan and has the sole authority to determine the meaning and application of the terms of the plan and all grant agreements, the persons to whom option or stock grants are made, the nature and amount of option or stock grants, the price to be paid upon exercise of each option, the period within which options may be exercised, the restrictions on stock awards, and the other terms and conditions of awards. All options granted under the 2000 Plan include accelerated vesting provisions in the event of a change in control, as defined in the plan. The 2000 Plan will terminate in February 2010. At December 31, 2001, 1, options were issued and outstanding and 1, 188, 320 options were available for issue under the 2000 Plan. The Company has granted stock options to officers, directors, and employees as follows.
Versus minimum effective concentration 10 4 M vitro cell death assay ; or quinoxaline derivatives of novel PARP-1 inhibitor, which we have recently identified Iwashita A., unpublished data ; . Cellular energy impairment seems to play an important part in MPTP-induced neurotoxicity. Striatal levels of NAD were decreased by 20% at 2 h after 4 times intraperitoneal injections of MPTP 20 mg kg ; in C57BL 6 mice. This partial loss of NAD seems to be selective for both the striatum nigrostriatal dopaminergic terminal field ; and the SNpc and was not observed in the cortex and hippocampus data not shown ; . Here, we investigated in vivo whether MPTP acutely caused region- and time-dependent changes in brain levels of NAD, and whether such effects were modified by treatment with neuroprotective doses of FR255595. Consistent with previous reports, neurotoxic doses of MPTP caused a rapid decrease in striatal NAD, DA metabolites Cosi and Marien, 1998 ; , and DAT binding affinity, and these changes were ameliorated by treatment with neuroprotective doses of and triptorelin.
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Bratman, David. Tolkien and the Counties of England.&& Mallorn 37 1999 ; 5 13. Bray, Lucy. Before and After.&& Mallorn 29 1992 ; 20. Bridoux, Denis. Of Amalion.&& Mallorn 23 1986 ; 1723. Broadwell, Elizabeth. Esse and Narn Name, Identity, and Narrative in the Tale of Tu; rin Turambar.&& Mythlore 64, 17.2 1990 ; 3440, 4244. Bullock, Richard P. The Importance of Free Will in The Lord of the Rings.&& Mythlore 41, 11.3 1985 ; 29, 5657. Burgess, Michael. From Genesis to Revelation in Middle-earth.&& Mallorn 22 1985 ; 4041. . Orome and the Wild Hunt The Development of a Myth.&& Mallorn 22 1985 ; 511. Burns, Marjorie J. J. R. Tolkien and the Journey North.&& Mythlore 58, 15.4 1989 ; 59. Callaway, David. Gollum A Misunderstood Hero.&& Mythlore 37, 10.3 1984 ; 1417, 22. Chausse, Jean. Icons of Jesus Christ in The Lord of the Rings.&& Mallorn 39 2001 ; 3032. Christensen, Bonniejean. Tolkien&s Creative Technique Beowulf and The Hobbit.&& Mythlore 57, 15.3 1989 ; 410. Christopher, Joe R. J. R. Tolkien, Narnian Exile Part I.&& Mythlore 55, 15.1 1988 ; 3745. . J. R. R. Tolkien, Narnian Exile Part II.&& Mythlore 56, 15.2 1988 ; 17 21. Clark, Craig. Problems of Good and Evil in Tolkien&s The Lord of the Rings.&& Mallorn 35 1997 ; 1519. Collings, Michael. Orson Scott Card An Approach to Mythopoeic Literature.&& Mythlore 81, 21.3 1996 ; 3650. Coombs, Jenny and Marc Read. Valaquenta and the Energy of the Valar.&& Mallorn 28 1991 ; 2935. Couch, Christopher L. From Under Mountains to Beyond Stars The Process of Riddling in Leofric&s The Exeter Book and The Hobbit.&& Mythlore 51, 14.1 1987 ; 913, 55. Craig, David M. Queer Lodgings& Gender and Sexuality in The Lord of the Rings.&& Mallorn 35 1997 ; 1118. Curry, Patrick. Magic vs. Enchantment.&& Mallorn 38 2001 ; 510. Curtis, Jenny. The Stone of Erech.&& Mallorn 24 1987 ; 1315. Cutsinger, James S. Angels and Inklings.&& Mythlore 72, 19.2 1993 ; 5760. Davidson, Christine. The Gorren A Tale of Later Years.&& Mallorn 21 1984 ; 2328. . Coming of Age Changes of Heart.&& Mallorn 39 2001 ; 1522.
And the PP samples were not significant [2 2 ; 4.006, P 0.135; 2 ; 3.319, P 0.190 respectively]. Abstinence rates during the last 6 weeks of treatment. As already mentioned, the abstinence rates for the periods between visits were recorded at each visit. An overview of the abstinence rates for the last 6 weeks of treatment is presented in Table 2. Statistical analyses were performed for three categories: abstinent, relapse, and missing. During the last 6 weeks of the 28-week treatment period, 18.2% of the ITT patients in group 1, 24.4% of group 2, and 17.9% of group 3 and trizivir.
Hydroxydiclofenac. Lack of involvement of further metabolites in diclofenac-induced mechanism-based inactivation was similar to the event in inactivation of CYP2C11 Masubuchi et al., 2001 ; . It has been demonstrated that benzoquinone imine, a further metabolite of 5-hydroxydiclofenac, is chemically reactive and binds covalently to cellular protein, suggesting the involvement of the toxicity of diclofenac Shen et al., 1999; Tang et al., 1999b ; . It is reasonable to speculate that reactive intermediates relevant to mechanism-based inactivation of CYP3A4 are too reactive to diffuse from the catalytic site of CYP3A4 and to bind other targets, whereas benzoquinone imine is relatively stable and can access to proteins other than P450s. The typical example revealing correlation between the stability and the target of a reactive metabolite is acetaminophen and its analog. Acetaminophen is a well known hepatotoxic compound, which is converted to a reactive benzoquinone imine and binds to hepatocellular proteins as the initial step of the toxicity, whereas its regioisomer, 3 -hydroxyacetanilide, is converted to a similar but highly reactive benzoquinone s ; , resulting in inactivation of P450 but not hepatotoxicity Halmes et al., 1998 ; . It is concluded that an intermediate during diclofenac 5-hydroxylation and a further metabolite of 5-hydroxydiclofenac lead to different toxicological consequences. We have not currently identified a chemical structure of the reactive metabolite to bind to CYP3A4, whereas arene-oxide is one of the possible candidates to be generated during diclofenac 5-hydroxylation. Because diclofenac 4 -hydroxylation by CYP2C9 does not result in its inactivation despite a higher metabolic rate than 5-hydroxylation, the two aromatic hydroxylations seem to proceed via distinct steps. In summary, it was found that diclofenac was a novel mechanismbased inactivator of CYP3A4. Quinidine, a stimulant of diclofenac 5-hydroxylation also stimulated inactivation of CYP3A4. 5-Hydroxydiclofenac was shown not to be a precursor of inactivating species; therefore, the 5-hydroxylation step is important in inactivation of CYP3A4.
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Your response to treatment. Travelling can be difficult for some patients, particularly if you live some distance away. The hospital does have accommodation which patients can use free of charge. If this is something you feel you need, please mention this to either the specialist nurse or the doctor looking after you. What are the early and temporary side effects of radiotherapy treatment? You will not feel anything during the treatment, however as you carry on with your treatment you may develop some side effects and these can worsen as you get closer to finishing.
Fibers throughout the rostrocaudal axis of the NTS. Although the possibility that irCART fibers observed in the NTS may be derived from other sources cannot be excluded, retrograde tract-tracing studies demonstrate that some of the irCART fibers in the NTS arise from neurons in the nodose ganglion. In our study, 50% of nodose ganglion cells that are Fluorogold positive are also irCART, which is consistent with a previous report that 50% of vagal afferents are irCART 3 ; . More interestingly, irCART nodose ganglion cells are generally of smaller diameter compared with Fluorogold and or CART-negative nodose neurons. Because of their small size, irCART nodose neurons that project to the NTS may belong to the slowly conducting type C neurons. It is pertinent to mention that not all nodose ganglion cells projecting to the NTS are baroreceptor afferents. Hence, not all irCART nodose ganglion cells projecting to the NTS are baroreceptor related. Intracisternal injection of CARTp consistently attenuated PE-induced bradycardia in a dose-dependent manner. CARTp injected intracisternally may reach a number of sites in the dorsal medulla that could potentially alter the cardiovascular response. To assess the role of NTS in relation to the action of CARTp, the peptide was injected directly into an area of NTS that is thought to be the predominant site of baroreceptor afferent termination 24 ; . CARTp injected into the NTS attenuated the PE-induced bradycardia in a dosedependent manner as well, suggesting that CARTp acts at the level of NTS. Our finding does not necessarily exclude the possibility that CARTp may act on other sites in the dorsal medulla to alter cardiovascular responses. Matsumura et al. 18 ; reported that CARTp by intracerebroventricular injection increased MAP, HR, and renal sympathetic nerve activity RSNA ; in conscious rabbits. Intracisternal or intraNTS administration of CARTp in the concentrations used in our study did not cause a significant change in basal arterial pressure or HR in anesthetized rats. Differences in experimental species and sites of administration as well as the observed time frame may have accounted for this discrepancy. Elevation of MAP and RSNA was observed 3040 min and increase of HR was observed 90 min after CARTp administration in rabbits, whereas in this study, the effect of CARTp reached its peak 10 min after injection in rats. Furthermore, CARTp was injected intracerebroventricularly, which may activate supramedullary neurons, leading to a different profile of cardiovascular responses in the case of rabbits. CARTp receptor antagonists are currently not available. CART antiserum, a rabbit polyclonal directed against the biologically active fragment CART55102 810 ; , was employed here to evaluate the pharmacological specificity of the effects of CARTp. Intra-NTS injections of CART antiserum augmented PE-induced bradycardia but did not produce a significant change in basal MAP or HR. If CARTp were tonically released, one would expect to see changes in baseline MAP and HR after CART antiserum. Because there were no significant changes in baseline activity, the peptide and trovafloxacin.
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W10 Goldberg HL, Finnery RJ. The use of doxepin in the treatment of symptoms of anxiety neurosis and accompanying depression: a collaborative controlled study. American Journal of Psychiatry 1972; 129 1 ; : 74-7. w11 Goldberg HL, Finnerty RJ, Cole JO. Doxepin: is a single daily dose enough? American Journal of Psychiatry 1974; 131 9 ; : 1027-9. w12 Goldberg HL, Finnerty RJ. Trazodone in the treatment of neurotic depression. Journal of Clinical Psychiatry 1980; 41 12Pt1 ; : 430-4. w13 Goldberg HL, Finnerty RJ, Cole JO. Doxepin: is a single daily dose enough? American Journal of Psychiatry 1974; 131 9 ; : 1027-9. w14 Hollanda Junior L, Silva CN, da, Lira BS, Ferreira SC. Double-blind clinical study with a new psychotropic agent: doxepin versus placebo. Hospital Rio Journal 1970; 77 3 ; : 799-803. w15 Hormazabal L, Omer LM, Ismail S. Cianopramine and amitriptyline in the treatment of depressed patients: a placebo-controlled study. Psychopharmacology 1985; 86 1-2 ; : 205-8. w16 Houston J, Berg I, Butler A, McGuire R. Amitriptyline for depressed women with young children in general practice. British Journal of Psychiatry 1983; 142: 103-4. w17 Jacobson AF. Doctor-patient concordance in a placebo-controlled trial of limbitrol versus its components proceedings. Psychopharmacology Bulletin 1978; 14 3 ; : 61-3. w18 Jenkins DG, Ebbutt AF, Evans CD. Tofranil in the treatment of low back pain. Journal of International Medical Research 1976; 4: 28-40. w19 Kerr MM. Amitriptyline in emotional states at the menopause. New Zealand Medical Journal 1970; 72 461 ; : 243-5. w20 Laederach-Hofmann K, Graf C, Horber F, Lippuner K, Lederer S, Michel R, Schneider M. Imipramine and diet counseling with psychological support in the treatment of obese binge eaters: a randomized, placebo-controlled double-blind study. International Journal of Eating Disorders 1999; 26 3 ; : 231-44. w21 Boyer P, Lecrubier Y. Atypical antipsychotic drugs in dysthymia: placebo controlled studies of amisulpride versus imipramine, versus amineptine. European Psychiatry: the Journal of the Association of European Psychiatrists 1996; 11 suppl 3 ; : S135-40. w22 Lecrubier Y, Boyer P, Turjanski S, Rein W. Amisulpride versus imipramine and placebo in dysthymia and major depression Amisulpride Study Group. Journal of Affective Disorders 1997; 43 2 ; : 95-103. w23 Macfarlane JG, Jalali S, Grace EM. Trimipramine in rheumatoid arthritis: a randomized double-blind trial in relieving pain and joint tenderness. Current Medical Research and Opinion 1986; 10: 89-93. w24 Morakinyo VO. Amytriptyline and chlordiazepoxide Limbitrol ; in depressive states in Nigeriansa double-blind study. African Journal of Medical Sciences 1970; 1 4 ; : 409-14. w25 Murphy JE, Donald JF, Molla AL. Mianserin in the treatment of depression in general-practice. Practitioner 1976; 217 1297 ; : 135-8. w26 Murphy JE. Mianserin in the treatment of depressive illness and anxiety states in general-practice. British Journal of Clinical Pharmacology 1978; 5 suppl 1 ; : 81S-5S. w27 Nandi DN, Ajmany S, Ganguli H, Banerjee G, Boral GC, Ghosh A, Sarkar S. A clinical evaluation of depressives found in a rural survey in India. British Journal of Psychiatry 1976; 128: 523-7. w28 Petracca G, Teson A, Chemerinski E, Leiguarda R, Starkstein SE. A double-blind placebo-controlled study of clomipramine in depressed patients with Alzheimer's disease. Journal of Neuropsychiatry and Clinical Neurosciences 1996; 8 3 ; : 270-5. w29 Philipp M, Kohnen R, Hiller K-O. Hypericum extract versus imipramine or placebo in patients with moderate depression: randomised multicentre study of treatment for eight weeks. British Medical Journal 1999; 319: 1534-8. w30 Rampello L, Nicoletti G, Raffaele R, Drago F. Comparative effects of amitriptyline and amineptine in patients affected by anxious depression. Neuropsychobiology 1995; 31 3 ; : 130-4. w31 Reifler BV, Teri L, Raskind M, Veith R, Barnes R, White E, McLean P. Double-blind trial of imipramine in Alzheimer's disease patients with and without depression. American Journal of Psychiatry 1989; 146 1 ; : 45-9. w32 Teri L, Reifler BV, Veith RC, Barnes R, White E, McLean P, Raskind M. Imipramine in the treatment of depressed Alzheimer's patients: impact on cognition. Journal of Gerontology 1991; 46 6 ; : P372-7. w33 Rickels K, Gordon PE, Jenkins BW, Perloff M, Sachs T, Stepansky W. Drug treatment in depressive illness. Diseases of the Nervous System 1970; 31 1 ; : 30-42. w34 Rickels K, Hesbacher P, Downing RW. Differential drug effects in neurotic depression. Diseases of the Nervous System 1970; 31 7 ; : 468-75. w35 Rickels K, Csanalosi I, Chung HR, Case WG, Pereira Ogan A, Downing RW. Amitriptyline in anxious-depressed outpatients: a controlled study. American Journal of Psychiatry 1974; 131 1 ; : 25-30. w36 Robertson MM, Trimble MR. The treatment of depression in patients with epilepsy A double-blind trial. Journal of Affective Disorders 1985; 9 2 ; : 127-36. w37 Rouillon F, Markabi S, Febvre N, Phillips R, Vaillant J. Controlled study of treatment of residual depression by clomipramine versus placebo. Encephale 1994; 20 2 ; : 139-45. w38 Schweizer E, Rickels K, Hassman H. A double-blind, placebo-controlled comparison of imipramine and buspirone in the treatment of major depression in the elderly in the community. Psychopharmacology Bulletin 1994: 639. w39 Schweizer E, Rickels K, Hassman H, Garcia Espana F. Buspirone and imipramine for the treatment of major depression in the elderly. Journal of Clinical Psychiatry 1998; 59 4 ; : 175-83. w40 Simpson GM, Pi EH, Gross L, Baron D, November M. Plasma levels and therapeutic response with trimipramine treatment of endogenous depression. Journal of Clinical Psychiatry 1988; 49 3 ; : 113-6. w41 Tan RS, Barlow RJ, Abel C, Reddy S, Palmer AJ, Fletcher AE, Nicholl CG, Pitt BM, Bulpitt CJ. The effect of low dose lofepramine in depressed elderly patients in general medical wards. British Journal of Clinical Pharmacology 1994; 37 4 ; : 321-4. w42 Tan RS. Lowering antidepressant dosages in the elderly. Clinical Gerontologist 1995; 16 1 ; : 67-70. w43 Tetreault L, Doucet P, Blanchet A, Bordeleau JM. Comparative evaluation of the antidepressive properties of opipramol, imipramine and placebo in neurotic depression. L'union Mdicale du Canada 1966; 95 5 ; : 546-53. w44 Thompson C, Thompson CM. The prescribing of antidepressants in general practice II: a placebo-controlled trial of low-dose dothiepin. Human Psychopharmacology 1989; 4: 191-204. w45 Tyrer P, Seivewright N, Murphy S, Ferguson B, Kingdon D, Barczak P, Brothwell J, Darling C, Gregory S, Johnson AL. The Nottingham study of neurotic disorder: comparison of drug and psychological treatments. Lancet 1988; 2: 235-40. w46 Tyrer P, Seivewright N, Ferguson B, Murphy S, Darling C, Brothwell J, Kingdon D, Johnson AL. The Nottingham Study of Neurotic Disorder: relationship between personality status and symptoms. Psychological Medicine 1990; 20 2 ; : 423-31. w47 Weissman MM, Prusoff B, Sholomskas AJ, Greenwald S. A double-blind clinical trial of alprazolam, imipramine, or placebo in the depressed elderly. Journal of Clinical Psychopharmacology 1992; 12 3 ; : 175-82. w48 Dose effects of antidepressant medication in different populations A World Health Organization collaborative study. Journal of Affective Disorders 1986; suppl 2 ; : 1-67. w49 Dose effects of antidepressant medication in different populations A World Health Organization collaborative study. Journal of Affective Disorders 1986; suppl 2 ; : 1-67. w50 Dose effects of antidepressant medication in different populations A World Health Organization collaborative study. Journal of Affective Disorders 1986; suppl 2 ; : 1-67. w51 Dose effects of antidepressant medication in different populations A World Health Organization collaborative study. Journal of Affective Disorders 1986; suppl 2 ; : 1-67 and trimipramine.
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Cylert ; — use of these medicines may increase the cnsstimulation read in stimulation ; effects of amphetamines and cause unwanted effects such asnervousness about nervousness ; , irritability more irritability ; , trouble trouble and drugs interaction ; insleeping sleeping and drugs interaction ; , and possiblyconvulsions convulsions and drugs interaction ; seizures ; appetite suppressants diet pills ; or medicine for asthma or otherbreathing about breathing ; problems or medicine for colds, sinus problems, or hayfever more fever ; or other allergies including nose drops or sprays ; — use of these medicines may increase the cns stimulation effects of amphetamines and cause unwanted effects such as nervousness, irritability, trouble in sleeping, or convulsions seizures ; , as well as unwanted effects on theheart see also heart ; andblood blood and drugs interaction ; vessels beta-adrenergic blocking agents acebutolol , atenolol , betaxolol , carteolol , labetalol , metoprolol , nadolol , oxprenolol , penbutolol , pindolol , propranolol , sotalol , timolol ; — use of amphetamines with beta-blocking agents may increase the chance of high bloodpressure see also pressure ; and heart problems cocaine— use by persons taking amphetamines may cause asevere read in severe ; increase in blood pressure and other unwanted effects, including about including ; nervousness, irritability, trouble in sleeping, or convulsions seizures ; digitalis glycosides heart medicine ; — amphetamines may cause additive effects, resulting inirregular irregular and drugs interaction ; heartbeat heartbeat and drugs interaction ; meperidine— use of meperidine by persons taking amphetamines is not recommended because the chance of serious side effects such as high fever, convulsions, or coma ; may beincreased more increased ; monoamineoxidase about oxidase ; mao ; inhibitor inhibitor and drugs interaction ; activity— isocarboxazid , phenelzine , procarbazine , selegiline , tranylcypromine ; — taking amphetamines while you are taking orwithin about within ; 2weeks see also weeks ; of taking monoamine oxidase mao ; inhibitors may increase the chance of serious side effects such as sudden and severe high blood pressure or fever thyroid hormones— the effects ofeither about either ; these medicines or amphetamines may be increased; unwanted effects may occur in patients with heart or blood vessel disease tricyclic antidepressants amitriptyline , amoxapine , clomipramine , desipramine , doxepin , imipramine , nortriptyline , protriptyline , trimipramine ; — although tricyclic antidepressants may be used with amphetamines to help make them work better, using the two medicines together may increase the chance of fast or irregular heartbeat, severe high blood pressure, or high fever othermedical medical and drugs interaction ; problems— the presence of other medical problems may affect the use of amphetamines.
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IT is hereby notified that pursuant to a resolution of the Board of Directors of the Bank of Ceylon adopted under Section 19 of the Bank of Ceylon Ordinance, published in the Gazette of the Democratic Socialist Republic of Sri Lanka No. 1204 of 28th September, 2001 and in the "Dinamina", "Thinakaran" and in the "Daily News" of 24.09.2001 Dunstan and Kelaart, Auctioneer of No. 381 1 Galle Road, Colombo 04, will sell by Public Auction on 16th February, 2002 at 10.30 a.m. at the spot, the property and premises described in the schedule hereunder for the recovery of the balance principal and interest due up to the date of sale land cost and monies recoverable under Section 26 of the siad Ordinance. SCHEDULE All that allotment of land bearing Assessment Nos. 140A, 140B situated along Colombo-Galle Road in Kollupitiya within the Municipality and District of Colombo Western Province and bounded on the North by a Lane, on the East by Main Road, Colombo to Galle on the South by property of W. M. Abdul Jaber bearing No. 129 and on the West by property of M. H. Abdul Cader and containing in extent One Rood and Thirty-two Decimal One Six Perches 0A., 1R., 32.16P. ; as per Plan No. 303 dated 19th June, 1928 made by M. L. Marikkar, Licensed Surveyor and registered in A601 34 at the Colombo District Land Registry. The above described allotment of land is according to a recent survey thereof No. 2062 dated 5th May, 1961 made by S. Rajendra, Licensed Surveyor is described as follows : All that and those the two contiguous allotments of land marked Lots 3 and 4 in the said Plan No. 2062 bearing Assessment No. 1, 9th Lane and 640, Kollupitiya Road, situated at Kollupitiya aforesaid together bounded on the North by 9th Lane on the East by Kollupitiya Road on the South by premises bearing Assessment No. 646, Kollupitiya Road and on the West by Lot 5 of the same land and containing in extent One Rood and Thirty-three Decimal One Five Perches 0A., 1R., 33.15P. ; . The above described allotment of land is according to a still more recent survey thereof No. 2273 dated 13th February, 1980 made by A. F. Sameer, Licensed Surveyor described as follows : All that allotment of land called Tekagahawatta together with the buildings standing thereon presently bearing Assessment No. 640, Kollupitiya Road and No. 1, 9th Lane situated at Kollupitiya in Ward No. 38, Bambalapitiya within the Municipality and District of Colombo Western bounded on the North by 9th Lane, on the East by Kollupitiya Road on the South by premises bearing Assessment Nos. 646, 1 and 646 5, Kollupitiya Road and West by premises bearing Assessment No. 15, 9th Lane, containing in extent One Rood Thirty-one Decimal Two Five Perches 0A., 1R., 31.25P. ; . By Order of the Board of Directors, Second Corporate Branch, Mrs. ; D. B. M. FERNANDO, Bank of Ceylon, Manager Recoveries. No. 4, Bank of Ceylon Mawatha, Colombo 01. 01-363 and ursinus.
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