Disease relevance of Ppr1

• RESULTS: Plasma pharmacokinetics of paclitaxel in patients with brain tumors were comparable to those previously described in patients with other malignancies [1].
• Coronavirus JHM: cell-free synthesis of structural protein p60 [2].
• METHODS: Plasma anti-CD40L antibodies from 125 patients with SLE, 24 with primary antiphospholipid syndrome (APS) and 90 with idiopathic thrombocytopenic purpura (ITP) and from 62 healthy individuals were measured with an enzyme-linked immunosorbent assay (ELISA) [3].
• METHODS: Plasma leptin, glucose and insulin, body weight, food intake, running wheel activity, and four adipose depots were measured in 587 adult F2 and backcross mice RESULTS: When mice were categorized by adiposity, a plot of food intake vs leptin illustrated a U-shaped curve [4].
• In 60 day old (P60) rats exposed to MAMac in utero, the latencies to myoclonic jerk (173 +/- 2.3 s) and forelimb clonus (215 +/- 4.6 s) were significantly shorter than those of controls (200 +/- 6.9 s and 238 +/- 8.8 s, respectively) [5].

Psychiatry related information on Ppr1

• Experiments were performed at different postnatal ages: postnatal day 12 (P12), before eye opening; P24, corresponding roughly to the peak of the critical period for monocular deprivation, and P60, after the end of the critical period [6].

High impact information on Ppr1

• To investigate the in vivo pathogenetic mechanisms of MTHFR deficiency, we generated mice with a knockout of MTHFR: Plasma total homocysteine levels in heterozygous and homozygous knockout mice are 1.6- and 10-fold higher than those in wild-type littermates, respectively [7].
• Granule cell number in P60 Grid2(Lc/)+;Bax-/- mice corresponded to 70% of the number found in wild-type mice [8].
• Ocular dominance columns form in ferrets between postnatal day 35 (P35) and P60 [9].
• Calpain Is Required for the Rapid, Calcium-dependent Repair of Wounded Plasma Membrane [10].
• Homer 1 Mediates Store- and Inositol 1,4,5-Trisphosphate Receptor-dependent Translocation and Retrieval of TRPC3 to the Plasma Membrane [11].

Chemical compound and disease context of Ppr1

• RESULTS: Plasma of women with pre-eclampsia, and interestingly, plasma of non-pregnant women, significantly enhanced myogenic tone at pressures > or =70 mmHg (P < 0.001) and blunted the maximum relaxation to methacholine (P < 0.001; P < 0.005) in isolated arteries [12].

Biological context of Ppr1

• The following markers of renal dysfunction and injury were measured: Plasma urea, creatinine, aspartate aminotransferase, and histology [13].
• RESULTS: Plasma and urine samples from mice 4 h after treatment with thalidomide contained eight major metabolites formed by hydroxylation and/or hydrolysis of thalidomide [14].
• In contrast, IGF-1 had no effect or even inhibited GnRH gene expression in adult P60 mice [15].
• The antibody response was predominantly targeted to the otherwise cryptic, conserved motif sequence in P60 [16].
• P32 was found to be genetically restricted to H-2(d) and H-2(b) haplotypes of mice, whereas P60 was found to be immunogenic in five different strains of mice [16].

Anatomical context of Ppr1

• Mice were fed 5 mg keyhole limpet hemocyanin (KLH) or 10 micrograms CT at least twice before parenteral immunization with 1 microgram KLH or CT in alum i.p. Plasma and intestinal secretions were collected at intervals [17].
• RECENT FINDINGS: Plasma concentrations of adiponectin, an adipocyte-specific protein, are reduced in obese subjects and in patients with type 2 diabetes and coronary artery disease [18].
• RESULTS: Plasma levels of leptin and adiponectin sharply decreased after 2 days of CLA feeding, although adipose tissue mass only decreased after day 6 [19].
• METHODS: Plasma proteins were fractionated by SDS-PAGE and immunoblots exposed to p75(NTR) antibody, using receptor protein from cultured PC12 cells as an external standard [20].
• METHODS: Plasma membrane potential (Vm) and currents were measured with microelectrodes or the patch-clamp technique; cytosolic Ca(2+) concentrations ([Ca(2+)](c)) and mitochondrial membrane potential (DeltaPsi) were measured using fluorescent dyes [21].

Associations of Ppr1 with chemical compounds

• RESULTS: Plasma glucose and insulin concentrations under basal and hyperinsulinaemic conditions were similar in MTII- and placebo-treated mice [22].
• RESULTS: Plasma corticosterone concentrations were dose dependently elevated by flesinoxan in wild type mice but not in knockout mice [23].
• RESULTS: Plasma elimination studies in mice indicated that the drug:drug ratio before injection [4:1 doxorubicin:vincristine (wt:wt ratio)] changed to 20:1 at the 24-h time point, indicative of more rapid release of vincristine from the liposomes than doxorubicin [24].
• EXPERIMENTAL DESIGN: Plasma from a NHL patient treated with Lym-1 was precipitated with ammonium sulfate and octanoic acid, followed by immunoadsorbant chromatography with solid phase Lym-1 monoclonal antibody to purify Ab2 [25].
• Both Tr and Pmp22tg mice show strongly reduced expression of genes important for cholesterol synthesis at P4, a characteristic that is common to all three mutants at P60 [26].

Regulatory relationships of Ppr1

• RESULTS: Plasma from these transgenic mice was capable of blocking PDGF-induced receptor autophosphorylation in tissue culture [27].
• CONCLUSIONS: Plasma CETP is posttranscriptionally downregulated in the lcat(-/-) mice, presumably by its extremely low HDL [28].
• RESULTS: Plasma total homocysteine was elevated with the high-methionine diet compared with the control diet for both Cbs+/+ (7.9+/-1.0 versus 5.0+/-0.5 micromol/L; P<0.05) and Cbs+/- (20.5+/-3.1 versus 8.2+/-0.9 micromol/L; P<0.001) mice [29].

Other interactions of Ppr1

• RESEARCH METHODS AND PROCEDURES: Plasma resistin, adiponectin, and leptin levels were examined in mice fed ad libitum, a 75% restricted diet, or a diet supplemented with 10% sucrose [30].
• METHODS: Plasma membranes were isolated from male wild-type (+/+) and mdr2 (-/-) mice for measurement of Na+-dependent taurocholate transport and assessment of Ntcp protein levels by Western blotting [31].
• On day 3, the ameliorative effects of CCR2 knockout were not observed; the increase in the urinary protein/creatinine ratio was similar in nephritic CCR2 wild-type (92 +/- 11.2) and knockout mice (102 +/- 9. 2). Plasma markers of disease were evaluated on days 4 and 7 [32].
• METHODS: Plasma corticosterone levels were determined in wild-type and p55-deficient mice that received systemic treatments with TNF-alpha and LPS, as well as exposure to auditory and restraint stressors [33].
• BACKGROUND: Plasma activity of semicarbazide-sensitive amine oxidase (SSAO) has been reported to be significantly higher in diabetic patients compared to healthy controls [34].

Analytical, diagnostic and therapeutic context of Ppr1

• METHODS: Plasma samples from lupus-prone (MRL/lpr and MRL/+) and control (CBA, Swiss, and BALB/c) mice were tested in enzyme-linked immunosorbent assays for the presence of nucleosomes, antinucleosome antibodies, and nucleosome-Ig complexes [35].
• METHODS: Plasma membrane potential and ion currents were measured with microelectrodes and the patch-clamp technique [36].
• RESULTS: Plasma ADMA and SDMA concentrations in members of the hypertensive group [0.23 +/- 0.03 and 1.37 +/- 0.06 micromol/l, respectively (means +/- SEM)] were significantly higher than those in members of the control group (ADMA 0.10 +/- 0.01 micromol/l and SDMA 1.18 +/- 0.06 micromol/l) [37].
• Retinal ganglion cells at ages P6 and P60 were purified by immunopanning, total RNA was extracted, and mRNA levels of the above proteins were determined by semiquantitative PCR [38].
• Embryos on embryonic day (E)10.5, E12.5, E15.5, and E18.5 and eyes from mice on postnatal day (P)0, P7, P11, P15, P30, and P60 were collected for immunofluorescence staining [39].

References