Dialog eLinks Full text available at Accession number & update 2007-05028-005 20070502. Source Psychology and Psychotherapy: Theory, Research and Practice! Other SerialTitle British Journal of Medical Psychology, Sep 2006, vol. 79, no. 3, p. 385-394, ISSN: 1476-0835. Publisher: British Psychological Society, United Kingdom. Author s ; Banerjee-Penelope, Duggan-Conor, Huband-Nick, Watson-Neil. Author affiliation Banerjee-Penelope, East Midlands Centre for Forensic Mental Health, Leicester, United Kingdom, penny.banerjee nottshc.nhs . Duggan-Conor, University of Nottingham, Division of Psychiatry, Nottingham, United Kingdom. Huband-Nick, Nottinghamshire Healthcare NHS Trust, Nottingham, United Kingdom. Watson-Neil, East Midlands Centre for Forensic Mental Health, Leicester, United Kingdom. Abstract journal abstract ; Background: The Patients' Charter for Mental Health Services DOH, 1997 ; states that a patient is entitled to both know and understand his or her diagnosis. Despite this, personality disordered clients are not always well informed about their disorder. Some will not be told their diagnosis because of concern that to do so would damage the therapeutic alliance. Objective: To test the hypothesis that the therapeutic alliance is not compromised by engaging in a psychoeducation programme that informs about personality disorder. Design: Pilot study, pre-post design. Methods: Eighteen forensic in-patients and 16 community out-patients separately participated in a 4-session individual programme that focused on personality, personality disorder, and their own diagnosis. Understanding of these concepts was explored in a brief structured interview. Therapeutic alliance was assessed pre- and post- intervention using the Agnew relationship measure. Results: For both samples, participation in the intervention resulted in a positive change in four of the five measured components of the therapeutic alliance. This change was rated more strongly by clients than therapists, and reached statistical significance for bond, partnership, and confidence subscales. Participants demonstrated improved knowledge of their disorder following the intervention, and all but one gave positive feedback. Conclusion: These findings support the hypothesis and suggest the therapeutic relationship is not impaired when a diagnosis of personality disorder is imparted using this psychoeducation programme. PsycINFO Database Record c ; 2007 APA, all rights reserved ; Grant Sponsorship: Nottinghamshire Healthcare NHS Trust supported this study. Tests and measures Agnew Relationship Measure; Wechsler Adult Intelligence Scale. Language English. Publication year 2006.
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A total of 57 subjects were genotyped for the Arg16 Gly16 -2 AR alleles. The observed allele frequencies of the -2 AR gene did not deviate from the Hardy-Weinberg equilibrium 2 0.176; P 0.67 ; . All 15 Gly16 homozygotes, all 12 Arg16 homozygotes, and 27 of 30 heterozygotes underwent hemodynamic measurements. The Table shows the clinical.
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Primary culture. Presented at the Satellite Symposium on "Functional aspects of energy metabolism in neural tissue", 1993 Annual Meeting of the International Society of Neurochemists, Carcassonne, France. 5. Lee, W-N. P., J. Edmond, S. Bassilian and J. W. Morrow. Mass isotopomer study of glutamate metabolism by astrocytes in primary culture. Presented at the Second International Conference on Brain Energy Metabolism, Blaubeuren, Germany, August, 1995. 6. Lee, W-N. P. The study of metabolic fluxes of the tricarboxylic acid cycle using carbon-13 tracers. Presented at the International Workshop on Design and Evolution of Metabolism, Tenerife, Spain, September 20-23, 1995. 7. Lee W-N P, Mao CS, Bassilian S, Lim S and EA Bergner. Study of Glucose Carbon Recycling, Cori Cycle and Gluconeogenesis Using [U13C]-glucose and Mass Isotopomer Analysis. Invited Presentation at the Symposium on In Vivo Measurement of Metabolic Processes, Prouts Neck, Maine, October, 1997. 8. Cascante M, Comin B, Boren J, Moro C, Martinez S, Centelles JJ, LeeW-N.P. and Boros L.G. Inhibition of tumor ribose-phosphate synthesis: A new strategy to control tumor proliferation. Plenary lecture at ComBio99, Darwin, Australia, 1999. 9. Boros, L.G., Go, V.L., Lee, W-N.P. Metabolic Profiling of Cell Growth and Death in Cancer. Presented at the Cambridge Healthtech Institute's Premier Conference on Metabolic Profiling: Pathways to Discovery Invited presentation, keynote address ; , Sheraton Chapel Hill Hotel, Chapel Hill, North Carolina, December 4, 2001. 10. Kurland I.J., J. Xu, G. Xiao, C. Pelayo, . F. Hernandez, A. Alcivar, B. Chung, S. Bassilian, M. Saad, W.N.P. Lee. Metabolic flux analysis using 13C mass spectrometry for the investigation of hepatic insulin signaling. Invited presentation ; Pathways in Discovery Conference, Chapel Hill, NC, December 3-4, 2001. 11. Lee WN P., L.G. Boros and CS Mao. Tracer Approaches to determining gluconeogenesis. Invited presentation, Nutrition Week 2003, San Antonio, TX, 2003. 12. Lee, WNP. Developing Risk Reduction Strategies through Metabolic Profiling. Invited presentation. Presented at Metabolic Profiling: Application to Toxicology and Risk Reduction, An International Conference Research Triangle Park, North Carolina, May 14-15, 2003. 13. Lee WNP, Wong D and Boros LG. The Nature of Metabolomics Data. Presented at the First International Meeting of the Metabolomics Society, Turuoka, Japan, June 2005. 14. Lee WNP and VLW Go. Nutrient-Gene Interaction: Tracer-Based Metabolomics. Invited presentation at the AICR WCRF International Research Conference on Food, Nutrition and Cancer, Washington DC, July 2005. 15. Lee WNP. Glucose Metabolic Phenotypes in Cancer. Invited presentation at the NCI Conference "Frontiers in Metabolomics for Cancer Research", Washington DC, October, 2005 Abstracts 1. Kirsch, J.K. and Lee, W.N.P. The chemical reactivity of hydroxy-trihydroborate anion: The reduction of esters and thioesters. Presented at the American Chemical Society Meeting, 1967. 2. Wimmer, R.J., Lee, W.N.P., Kaplan, S.A. and Greenfield, M.A. Estimation of absolute iodide uptake AIU ; with I-123 by coincidence counting. Presented at the American Radiological Society of North America Meeting, December 1975. 3. Lee, W.N.P., Wimmer, R.J., Kaplan, S.A. and Greenfield, M.A. I-123 early radioiodine uptake test as a prediction of outcome in children with thyrotoxicosis. Pediatr. Res. 11: 428, 1977.
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MINN. STAT. ANN. 152.02 West 2004 ; Schedules of controlled substances; administration of chapter Subdivision 1. Five schedules. There are established five schedules of controlled substances, to be known as Schedules I, II, III, IV, and V. Such schedules shall initially consist of the substances listed in this section by whatever official name, common or usual name, chemical name, or trade name designated. Subd. 2. Schedule I. The following items are listed in Schedule I: 1 ; Any of the following substances, including their isomers, esters, ethers, salts, and salts of isomers, esters, and ethers, unless specifically excepted, whenever the existence of such isomers, esters, ethers and salts is possible within the specific chemical designation: Acetylmethadol; Allylprodine; Alphacetylmethadol; Alphameprodine; Alphamethadol; Benzethidine; Betacetylmethadol; Betameprodine; Betamethadol; Betaprodine; Clonitazene; Dextromoramide; Dextrorphan; Diampromide; Diethyliambutene; Dimenoxadol; Dimepheptanol; Dimethyliambutene; Dioxaphetyl butyrate; Dipipanone; Ethylmethylthiambutene; Etonitazene; Etoxeridine; Furethidine; Hydroxypethidine; Ketobemidone; Levomoramide; Levophenacylmorphan; Morpheridine; Noracymethadol; Norlevorphanol; Normethadone; Norpipanone; Phenadoxone; Phenampromide; Phenomorphan; Phenoperidine; Piritramide; Proheptazine; Properidine; Racemoramide; Trimeperidine. 2 ; Any of the following opium derivatives, their salts, isomers and salts of isomers, unless specifically excepted, whenever the existence of such salts, isomers and salts of isomers is possible within the specific chemical designation: Acetorphine; Acetyldihydrocodeine; Acetylcodone; Benzylmorphine; Codeine methylbromide; Codeine-N-Oxide; Cyprenorphine; Desomorphine; Dihydromorphine; Etorphine; Heroin; Hydromorphinol; Methyldesorphine; Methylhydromorphine; Morphine methylbromide; Morphine methylsulfonate; Morphine-N-Oxide; Myrophine; Nicocodeine; Nicomorphine; Normorphine; Pholcodine; Thebacon. 3 ; Any material, compound, mixture or preparation which contains any quantity of the following hallucinogenic substances, their salts, isomers and salts of isomers, unless specifically excepted, whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation: 3, 4-methylenedioxy amphetamine; 3, 4- methylenedioxymethamphetamine; 4bromo-2, 5-dimethoxyamphetamine; 2, dimethoxyamphetamine; 4-methoxyamphetamine; 5methoxy-3, 4-methylenedioxy amphetamine; Bufotenine; Diethyltryptamine; Dimethyltryptamine; 3, 4, 5- trimethoxy amphetamine; 4-methyl-2, 5-dimethoxyamphetamine; Ibogaine; L6sergic acid diethylamide; marijuana; Mescaline; N-ethyl-3-piperidyl benzilate; N-methyl-3-piperidyl benzilate; Psilocybin; Psilocyn; Tetrahydrocannabinols; 1- 2-thienyl ; cyclohexyl ; piperidine; n-ethyl-1phenyl-cyclohexylamine; 1- 1-phenylcyclohexyl ; pyrrolidine. 4 ; Peyote, providing the listing of peyote as a controlled substance in schedule I does not apply to the nondrug use of peyote in bona fide religious ceremonies of the American Indian Church, and members of the American Indian Church are exempt from registration. Any person who manufactures.
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And felony conviction. Agreed Board Order accepted by licensee and entered by the Board on 8-6-03: probation to run concurrent with probation imposed on licensee's OK pharmacist license. Emeka C. Alozie, License No. 35700, Missouri City, TX. Alleged violations: felony conviction; maintained outdated drugs in dispensing stock; maintained samples; failed to keep records and reference library, and failed to label prescription container with the words "substituted for brand prescribed" when substituting generic drug for the brand prescribed. Agreed Board Order accepted by licensee and entered by the Board on 2-5-03: probation concurrent with criminal probation, under conditions; may not serve as a pharmacist-in-charge of any pharmacy; and may not own a pharmacy. Richard Jay Daniel, License No. 21180.
Arrive at clinic at designated time with proper photo ID. Sign in. Read entire Task Card. Receive briefing from Education Forms Team Leader. Set up educational materials. Provide educational materials FAQ sheets. Answer client questions regarding agent, what they can expect. Read the intake form for individuals who are unable to read. Work with interpreters to assist non-English speaking individuals Direct clients to Medical Screening 1. Refer clients to Medical Screening 2 if they have more complex questions. Debrief with Education Forms Team Leader and brief replacement. Assist with demobilization, as directed. Sign out and mescaline.
An IBD implementation quality improvement team uses this IBD Guideline to help optimize evidence-based care. The clinic forms and treatment algorithms are being piloted and continuously improved to achieve best clinical outcomes. Parents have been working with CCHMC implementation improvement teams to optimize EBC for their children as evident by their participation in testing the child parent clinic assessment forms Appendix 1C, 1D, 1E. A search using the above criteria will be conducted at least once per year in search of any "invalidating evidence" that may be used as potential future citations for the guideline. If any "invalidating evidence" is found , the development team will review the evidence and or reconvene to further explore the continued validity of the guideline and or address the revision of recommendations as needed. This phase can also be initiated at any point that new evidence indicates a critical change is needed. Recommendations have been formulated by a consensus process directed by best evidence, patient and family preference and clinical expertise. During formulation of these recommendations, the team members have remained cognizant of controversies and disagreements over the management of these patients. They have tried to resolve controversial issues by consensus where possible and, when not possible, to offer optional approaches to care in the form of information that includes best supporting evidence of efficacy for alternative choices. The guidelines have been reviewed and approved by clinical experts not involved in the development process, senior management, other appropriate hospital committees, and other individuals as appropriate to their intended purposes. The guideline was developed without external funding. All Team members and Clinical Effectiveness support staff listed have declared whether they have any conflict of interest and none were identified. Copies of this Evidence-based Care Guideline EBCG ; and its companion documents are available online and may be distributed by any organization for the global purpose of improving child health outcomes. Website address!
Centrations below 1 M and without changes in baseline current, arguing against an involvement of the ligand-gated 5-HT3 receptor. Consistent with these results, selective 5-HT3 receptor antagonists did not inhibit enhancement of TRPV1 function by 5-HT, revealing that activation of metabotropic 5-HT receptors facilitates TRPV1 responses. To establish this experimentally, we blocked G-protein-coupled signaling pathways by adding GDP-S to the pipette solution, which abolished TRPV1 modulation by 5-HT. We found that activation of both 5-HT2 and 5-HT4 and methamphetamine.
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Participating in these studies have been Gloria Faretra, M.D., Psychiatrist; D. V. Siva Sankar, Ph. D., Biochemist; Leonard Cobrinik, Ph.D. Psychologist; Lothar Goldschmidt, IV[. D., Psychiatrist; and many others. A current, still unpublished study, is being done by Lillian Dooher, M.D., Jean Dowling, M. IY., and Don Winn. M. D. REFERENCES 1. Bender, L., Goldschmidt, L., Sankar, S.: Treatment of autistic chizophrenic s children with LSD-25 and UML-491. In Wortis, J., ed. Recent Advances in Biological Psychiatry. Vol. IV. Plenum Press, New York, 1962. 2. Bender, L., Faretra, G., and Cobrinik, L.: LSD and UML treatment of hospitalized disturbed children In Wortis, J., ed., Recent Advances in Biological Psychiatry, Voi. V. Plenum Press, New York, 1963. 3. Bender, L., et. al.: The treatment of childhood schizophrenia with LSD and UML In Rinkel M. ed., "Biological Treatment of Mental Illness Lic. Page. New York, 1966. 4. Bender, L.: Concept of plasticity in childhood schizophrenia. In Hoch, P. and Zubin, J., eds., Schizophrenia. Grune and Stratton, New York, 1966. 5. Brodie, B.B.: Interaction of psychotropic drugs with physiologic and biochemical mechanisms in the brain. Modern Med., 6980, 1958. 6. Dalessio, D.J.: On migraine headache: Serotonin and serotonin antagonism. J.A.M.A. 181: 318-321, 1961. Faretra, G., and Bender. L.: Autonomic nervous system responses in hospitalized children treated with LSD and UlVIL. In Wortis, J., ed., Recent Advances in Biological Psychiatry, Vol. VII, 1964. 8. Huxley, A.: Doors of Perception. Harper & Bros., New York, 1954. 9. Kety, S.S.: Biochemical theories of schizophrenia. Internat'l J. Psychiat. 1: 409-446, 1965 reprint ; . 10. Sankar, lY.V.S., Broer, H.H., and Cates, N.: Studies on biogenic amines and psychoactive drug actions, with special references to lysrrgic acid diethyl amide. Transav. N.Y. Acad. o Sci., 26: 369-376, 1964. Sankar, D.V.S., et. al.: Biochemical parameter in childhood schizophrenia autism ; and growth. In Wortis, J., ed., Recent Advances in Biological Psychiatry. Plenum Press, New York, 1963. 12. Schain, R. J., and Freedman, D. X.: Studies on 5-hydroxy indole metabolism in autistic sand other mentally retarded children. J. Pediat. 58: 315-321, 1961. Wolf, H.G., Dalessio, D., Camp, W.A., and Goodill, H.: Studies on headaches: The mode of action in U'ML-491. Arch. Neut, & Psychiat. 4: 235-240, 1961.
The biochemical diagnosis of 2 hyperparathyroidism relies since approximately 20 years on the determination of plasma intact PTH. This is true for 1 and 2 forms of hyperparathyroidism. In patients with CRF, it has however become apparent in recent years that there are some limitations for intact PTH in plasma. Normal intact PTH plasma values are not normal for uremic patients since values in the normal range are generally associated with low bone turnover adynamic bone disease ; whereas normal bone turnover may be observed in presence of elevated plasma intact PTH levels . It is currently unclear to what extent this is due to imperfections in the PTH assays used see below ; , PTH receptor state, post-receptor events, non-PTHmediated changes in bone metabolism e.g. supply of vitamin D or its metabolites, supply of estrogens or androgens ; , or a combination of these factors. The accumulation of a large non 1-84 ; molecular form of PTH, which is detected by intact PTH assays, has been described in patients with CRF . The large PTH fragment was tentatively identified as hPTH 7-84 ; . This finding is of importance in the interpretation of PTH values, since true hPTH 1-84 ; represents only about 50-60% of the levels detected by the currently used intact PTH assays, and since PTH 7-84 ; antagonizes PTH 1-84 ; effects on serum calcium and on osteoblasts . Moreover, the secretory responses of hPTH 1-84 ; and non-hPTH 1-84 ; to changes in extracellular calcium concentration are not proportional for these two PTH moieties . A novel immunoradiometric assay has been developed which detects full-length whole ; human PTH, but not amino-terminally truncated fragments . Monier-Faugere et al proposed to further improve the assessment of uremic hyperparathyroidism and the associated increase in bone turnover by calculating the ratio of PTH- 1-84 ; to large C-PTH fragments . The usefulness in the clinical setting of the whole PTH assay or of the ratio of whole PTH to PTH fragments has however not been established at present for the diagnosis of parathyroid overfunction in adult dialysis patients or pediatric dialysis patients . The radiological diagnosis is relatively easy in advanced stages of 2 hyperparathyroidism. Typical lesions include resorptive defects on the external and internal surfaces of cortical bone, particularly resorption on the subperiosteal surface. Resorption within cortical bone enlarges the Haversian channels, resulting in longitudinal striation; resorption at the endosteal surface causes cortical thinning. These lesions 22 and methylphenidate.
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Lysergic Acid Xulfate-100 mg. of lyserhic acid were dissolved in 8 cc. of hot water and a slight excess of dilute HzS04 was added. Upon cooling the sulfate separated as leaflets. It was recrystallized from 6 cc. of hot water. It melts with decomposition at about 220, depending somewhat upon the rate of heating. It was dried for analysis at 120' and 2 mm.
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Mdma indicates methylenedioxymethamphetamine; dmt, dimethyltryptamine; 5-meo-dmt, 5-methoxy-dimethyltryptamine; 5-meo-dipt, n, n-diisopropyl-5-methoxy; lsd, lyseric acid diethylamide; pcp, phencyclidine; ghb, -hydroxybutyrate; 2-ct7, 2, 5-dimethoxy-4- n ; -propylthiophenethylamine; 2-cb, 4-bromo-2, 5-dimethoxyphenethylamine and methylprednisolone.
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