Disease relevance of AMDP1

• AMD activity levels, however, correlated with tumor malignancy only up to grade III astrocytoma [1].
• Medulloblastomas exhibited an unusual dichotomy with regard to the levels of polyamine biosynthetic decarboxylases (PBD): Medulloblastomas had the highest ODC activities of all the CNS tumors tested but had low AMD activities [1].
• However, atypical forms of meningioma, i.e., those with mitotic figures, whatever the histologic variants, had higher levels of ODC, but not of AMD, than the typical forms, i.e., those without mitotic figures [1].
• In tumors of neuroepithelial tissue ODC level increases and, when present, AMD level increases were not due to proliferation of new blood vessels, because CNS hemangioblastomas had very low levels of both PBD activities [1].
• Age-related macular degeneration (AMD; OMIM #603075) is the most frequent cause of visual impairment in the elderly population, with severe disease affecting nearly 10% of individuals of European descent over the age of 75 years [2].

Psychiatry related information on AMDP1

• Positive and negative symptoms and extrapyramidal side effects were assessed using standardized rating scales (PSAS, AMDP, SANS). 'Reaction time' and 'motor speed' were measured using a computer-aided system and striatal dopamine D2/D3 receptor availability was assessed using [I-123]IBZM SPECT [3].
• In an AMDP training seminar on psychopathology, the possible learning effects were studied [4].
• The effect of monocular (MD), binocular (BD) and alternating monocular (AMD) deprivation on monocular pattern discrimination learning and interocular transfer was investigated in pigeons reared with intact and sectioned supraoptic decussation (DSO) [5].
• A total of 364 schizophrenic outpatients who were stabilized for 3 months on continuous neuroleptic therapy after discharge from the hospital were rated according to three different scales for depressive syndromes (Brief Psychiatric Rating Scale anxious depression factor, AMDP/depression, and the self-rating PD-S depression scale) [6].
• Initial affective symptoms had been extracted from clinical records according to a standardized system (AMDP) [7].

High impact information on AMDP1

• Detailed analysis showed a common haplotype associated with decreased risk of AMD that was present on 20% of chromosomes of controls and 8% of chromosomes of individuals with AMD [2].
• Consistent with these findings, we show that pharmacologic elevation of cAMP with the phosphodiesterase inhibitor Rolipram suppresses tumor cell growth in vitro and, upon oral administration, inhibits intracranial growth in xenograft models of malignant brain tumors with comparable efficacy to AMD 3465 [8].
• We discovered that CXCL12-dependent tumor growth is dependent upon sustained inhibition of cyclic AMP (cAMP) production, and that the antitumor activity of the specific CXCR4 antagonist AMD 3465 is associated with blocking cAMP suppression [8].
• PATIENTS AND METHODS: Eligible patients (N = 509) had received four weekly doses of vincristine (VCR) and two courses of dactinomycin (AMD) preoperatively and were assigned after surgery, according to stage and lymph node involvement, to three different prognostic groups, which were to be randomized [9].
• Stage IIN1 and III patients (n = 83) received intensified VCR and AMD (INTVCR) versus VCR, AMD, and Adriamycin (ADRIA; Doxorubicin Farmitalia Carbo Erba, Rueil, Malmaison, France; doxorubicin) [9].

Chemical compound and disease context of AMDP1

• Elderly human subjects with and without AMD can safely take supplements of lutein up to 10 mg/d for 6 months with no apparent toxicity or side effects [10].
• RESULTS: In the 291 eyes analyzed, NIR fluorescence was observed in 51 and was graded weak in 27 with wet age-related macular degeneration (AMD, 10 cases), dry AMD with pigment clumping (n=7), chronic central serous choroidopathy (CSC; n=5), choroidal nevi (n=2), subretinal hemorrhages (n=2), and chloroquine maculopathy (n=1) [11].
• Under NL (A), after 12 days NL-withdrawal (B), after 15 (C) and 30 (D) days Nicergoline treatment clinical ratings (BPRS and AMDP) and stimulation with clonidine (0.002 micrograms/kg body weight) were carried out [12].
• To verify the adequacy of a simplified chemotherapeutic regimen for the treatment of Wilms' tumor (WT), the authors conducted a clinical trial to compare the standard fractionated dose (15 mcg/kg x 5 days) of dactinomycin (AMD) with a single dose (60 mcg/kg x 1 day) administration of the drug [13].
• We have determined the levels of L-ornithine decarboxylase (ODC) and S-adenosyl-L-methionine decarboxylase (AMD) in 134 untreated human primary tumors, such as skin epitheliomas and brain tumors [14].

Biological context of AMDP1

• The third AMD locus (AMD3) in FM3A cells contains a pseudogene, in which deletion of two bases generates a premature termination codon at position 57 [15].
• After transient transfection in various cell lines, the AMD1 promoter was one to two orders of magnitude stronger than the AMD2 promoter [15].
• The promoter regions of two S-adenosylmethionine decarboxylase genes (AMD genes) were isolated from a mouse genomic library [15].
• AMD1 was localized to chromosome region 6q21-->q22 and AMD2 to band Xq28 [16].
• We now report characterization of the AMD2 locus (GenBank Accession No. U02035) on the X chromosome, which contains sequences that cross-hybridize with human AdoMetDC cDNA [16].

Anatomical context of AMDP1

• Historical descriptions of the involvement of inflammatory cells are provided, evidence implicating inflammation in the pathogenesis of AMD involving macrophages, giant cells and microglia has been derived from observations of human and animal subretinal neovascular lesions [17].
• Altogether, our results show that polyplexes formulated with AMD-labeled polymers constitute, under certain conditions, specific gene transfer systems into suspension CXCR4(+) Jurkat cells [18].
• Although lymphocytes take up less 3H-AMD than CH cells, the differential inhibitory effect of AMD on nucleic acid synthesis in the two cell types is small [19].
• The glycogen synthase phosphatase activity, measured from the rate of activation of liver glycogen synthase, is virtually accounted for by AMD phosphatases; the bulk of the activity belongs to the glycogen-bound protein phosphatase G and a small part is present in the cytosol [20].
• Pyramidal tract diffusion characteristics of patients with ALS or adrenoleukodystrophy of AMD type were relatively intact suggesting a pathological process characterized by relatively preserved structural architecture [21].

Associations of AMDP1 with chemical compounds

• The human S-adenosylmethionine decarboxylase gene: nucleotide sequence of a pseudogene and chromosomal localization of the active gene (AMD1) and the pseudogene (AMD2) [16].
• The separation of acyclovir (ACV) by high performance capillary electrophoresis (HPCE) with on-column amperometric detection using alpha-amino-5-mercapto-3,4-dithiazole (AMD) as internal standard is described [22].
• The concentrations of platelet 5-HT level did not correlate with either plasma TRP or with clinical variables, that is, AMDP depression and AMDP anxiety scores [23].
• This is more particularly the case when the nonspecific transfection pathways are minimized (i.e. for N/P <or= 2.5 AMD-labeled polyplexes) and in the presence of phorbol myristate acetate which triggers CXCR4 receptor endocytosis of the AMD-labeled polyplexes to a larger extent than that of their respective nonlabeled ones [18].
• Based on cell counts AMDP (IC50, 8 and 11 microM in SW707 and SW948, respectively) and DADP (IC50, 266 and 285 microM in SW707 and SW948, respectively) showed more intensive antiproliferative efficacy as determined by the Coulter Counter method vs the MTT assay [24].

Analytical, diagnostic and therapeutic context of AMDP1

• When transcription was inhibited under physiological conditions (mitosis) or after AMD treatment the antigen remained, as shown by immunoblotting and immunolabeling with anti-NOR serum [25].
• METHODS: AF [787] fundus images (excitation [Exc.] 787 nm; emission [Emi.] >800 nm) were recorded with a confocal scanning laser ophthalmoscope, in 85 normal subjects (ages: 11-77 years) and in 25 patients with AMD and other retinal diseases [26].
• METHODS: This was a retrospective study. fmERGs were recorded in 19 eyes of 19 consecutive patients who underwent macular translocation with 360 degrees retinotomy for choroidal neovascularization (CNV) secondary to age-related macular degeneration (AMD; 17 eyes) or polypoidal choroidal vasculopathy (2 eyes) [27].
• From our study and from a similar report in the literature (de Barsy et al., 1975), it appears that a combined approach of light microscopy, electron microscopy and biochemical analysis (determination of acid alpha-glucosidase) is necessary to make a diagnosis of AMD in adults [28].
• AIMS: The risk of smoking habits for developing the neovascular form of age related macular degeneration (neovascular form of AMD) were studied by a case-control study in Japan. METHODS: 56 male patients with the neovascular form of AMD and 82 healthy male controls, aged 50 to 69 years, were enrolled [29].

References