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PubMed1996

Cytotoxicity, pH, and glucose degradation products in four different brands of PD fluid.

This study was undertaken in order to evaluate differences in pH, cytotoxicity, and concentration of glucose degradation products between different peritoneal dialysis (PD) fluids. Four brands of commercial PD fluids were selected: Gambrosol, Bieffe, Dianeal, and Lock-olys, with a glucose concentration between 3.86% and 4.25%. The cytotoxicity of unused PD fluid was measured as inhibition of cell growth after three days' exposure of a fibroblast cell line using neutral red vital stain. The concentration of 2-furaldehyde, 5-hydroxymethyl-furaldehyde (5-HMF), acetaldehyde, formaldehyde, glyoxal, and methylglyoxal was analyzed by high-performance liquid chromatography technique. All the investigated PD fluids were cytotoxic and contained noticeable amounts of aldehydes. No major differences were observed in pH, although one fluid with a slightly lower pH was found to be less cytotoxic. This fluid also contained less formaldehyde, acetaldehyde, methylglyoxal, and glyoxal but instead contained more 5-HMF. We conclude that all brands of PD fluid are cytotoxic due to glucose degradation products and that they contain noticeable concentrations of low-molecular aldehydes. Our results also demonstrate that the concentration of 5-HMF, used as a regulatory control of PD fluids, does not correlate well with cytotoxicity.

Acid-Base Equilibrium↗
PubMed1997

Effects of D3-preferring agonists 7-OH-PIPAT and PD-128,907 on motor behaviors and place conditioning.

Dose-dependent effects of 7-OH-PIPAT and PD-128,907 on motor behaviors and place conditioning were examined in rats. Four 2-day conditioning trials were conducted over 8 consecutive days. On one day of each trial, animals received an injection of either saline, one of six doses of 7-OH-PIPAT (0.01-10.0 mg/kg), or one of five doses of PD-128,907 (0.01-1.0 mg/kg), and were placed into a distinct compartment for 40 min. On the other day, animals received an injection of saline and were placed into a different compartment for 40 min. Locomotion, sniffing, and yawning were measured following the first and last drug injections. Place conditioning was assessed the day following the last conditioning trial. None of the doses of 7-OH-PIPAT or 0-0.3 mg/kg PD-128,907 produced place conditioning. However, 1 mg/kg PD-128,907 produced conditioned place preference (CPP). Across doses, both 7-OH-PIPAT and PD-128,907 produced a U-shaped change in sniffing and locomotion and an inverted U-shaped change in yawning. Across time, lower doses produced a decrease in sniffing and locomotion and an increase in yawning that were evident immediately, whereas higher doses produced a biphasic change in that there was an initial decrease followed by an increase in sniffing and locomotion. Behaviors produced by both low and high doses were sensitized following repeated administration. PD-128,907 produced CPP and was more potent than 7-OH-PIPAT in altering motor behaviors, possibly due to its greater selectivity for the D3 receptor.

Animals↗
PubMed1984

The relationship between WAIS PA and MMPI SI is mediated by MMPI PD.

Investigated the effects of MMPI PD on the relationship between WAIS PA and MMPI SI. WAIS PA performance and MMPI SI have been reported to be related negatively in university undergraduates (Schill, 1966) and related positively in psychiatric patients (Johnson, 1969). This study was derived from the assumption that Schill's undergraduates had higher MMPI PD than Johnson's patients. Data from 65 psychiatric hospital patients showed that the PA - SI relationship was negative in high PD Ss and positive in low PD Ss, in support of this assumption. Thus, WAIS PA performance does have clinical implications for assessing social involvement, but the interpretation of PA depends on MMPI PD.

Adult↗
PubMed2002

Local photodynamic therapy (PDT) of rat C6 glioma xenografts with Pd-bacteriopheophorbide leads to decreased metastases and increase of animal cure compared with surgery.

Photodynamic therapy (PDT), locally applied to solid C6 rat glioma tumors in the foot of CD1 nude mice, eradicated the primary tumor and also decreased the rate of groin and lung metastases. Pd-Bacteriopheophorbide (Pd-Bpheid), a novel photosensitizer synthesized in our laboratory, was used in our study. The primary lesion in the hind leg was treated by an i.v. injection of 5 mg/kg of Pd-Bpheid and immediate illumination (650-800 nm, 360 J/cm(2)). This protocol and the surgical amputation of the leg were compared for local and metastasis responses. Following PDT, hemorrhage, inflammation with tumor necrosis and flattening were observed and histologically verified in the photodynamically treated tumor. Whereas local tumor control rates were up to 64% following PDT, in surgically treated animals, local tumor control was absolute. The rates of metastases in the groin and the lungs were at least 12-fold lower in the photodynamically treated animals compared with untreated or surgery-treated groups. The overall cure rates after PDT or surgery were 36% and 6%, respectively, at 8 weeks. These findings suggest that local PDT with Pd-Bpheid, which acts primarily on the tumor vasculature, efficiently eradicates the solid C6 tumors. In addition, the local PDT of the primary lesion has beneficial therapeutic effects on remote C6 metastasis, which is not obtained with surgery. It is therefore suggested, that although surgery is highly efficient for the immediate removal of the primary tumor, it lacks such systemic, therapeutic effects on distant metastases. Pd-Bpheid-PDT may thus offer a potentially superior curative therapy for C6 glioma tumors in the limb by eradicating the target tumor and by reducing the rate of metastasis in the groin and lung, possibly due to innate immunity.

Animals↗
PubMed1992

Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death.

The classical type of programmed cell death is characterized by its dependence on de novo RNA and protein synthesis and morphological features of apoptosis. We confirmed that stimulated 2B4.11 (a murine T-cell hybridoma) and interleukin-3 (IL-3)-deprived LyD9 (a murine haematopoietic progenitor cell line) died by the classical type of programmed cell death. Assuming that common biochemical pathways might be involved in the deaths of 2B4.11 and LyD9, we isolated the PD-1 gene, a novel member of the immunoglobulin gene superfamily, by using subtractive hybridization technique. The predicted PD-1 protein has a variant form of the consensus sequence found in cytoplasmic tails of signal transducing polypeptides associated with immune recognition receptors. The PD-1 gene was activated in both stimulated 2B4.11 and IL-3-deprived LyD9 cells, but not in other death-induced cell lines that did not show the characteristic features of the classical programmed cell death. Expression of the PD-1 mRNA in mouse was restricted to the thymus and increased when thymocyte death was augmented by in vivo injection of anti-CD3 antibody. These results suggest that activation of the PD-1 gene may be involved in the classical type of programmed cell death.

Amino Acid Sequence↗
PubMed2005

Au(III), Pd(II), Ni(II), and Hg(II) alter NF kappa B signaling in THP1 monocytic cells.

The transcription factor NFkappaB plays a key role in the tissue inflammatory response. Metal ions released into tissues from biomaterials (e.g., Au, Pd, Ni, Hg) are known to alter the binding of NFkappaB proteins to DNA, thereby modulating the effect of NFkappaB on gene activation and, ultimately, the tissue response to biomaterials. Little is known about the effect of these metals on key signaling steps prior to NFkappaB-DNA binding such as transcription factor activation or nuclear translocation, yet these steps are equally important to modulation of the pathway. Oxidative stress is known to alter NFkappaB proteins and is suspected to play a role in metal-induced NFkappaB signaling modulation. Our aim in the current study was to assess the effects of sublethal levels of Ni, Hg, Pd, and Au ions on NFkappaB activation and nuclear translocation in the monocyte, which is acknowledged as an important orchestrator of the biological response to materials and the pathogenesis of chronic disease. Sublethal concentrations of Au(III), Ni(II), Hg(II), and Pd(II) were added to cultures of human THP1 monocytic cells for 72 h. In parallel cultures, lipopolysaccharide (LPS) was added for the last 30 min to activate the monocytic cells. Then cellular cytoplasmic and nuclear proteins were isolated, separated by electrophoresis, and probed for IkappaBalpha degradation (activation) and NFkappaB p65 translocation. Protein levels were digitally quantified and statistically compared. The levels of reactive oxygen species (ROS) in the monocytic cells were measured as a possible mechanism of metal-induced NFkappaB modulation. Only Au(III) activated IkappaBalpha degradation by itself. Au(III) and Pd(II) enhanced LPS-induced IkappaBalpha degradation, but Hg(II) and Ni(II) suppressed it. Au(III), Ni(II), and Pd(II) activated p65 nuclear translocation without LPS, and all but Ni(II) enhanced LPS-induced translocation. Collectively, the results suggest that these metal ions alter activation and translocation of NFkappaB, each in a unique way at unique concentrations. Furthermore, even when these metals had no overt effects on signaling by themselves, all altered activation of signaling by LPS, suggesting that the biological effects of these metals on monocytic function may only be manifest upon activation. None of the metal ions elevated levels of ROS at 72 h, indicating that ROS were probably not direct modulators of the NFkappaB activation or translocation at this late time point.

Cations, Divalent↗
PubMed2006

Estrogen-mediated immunomodulation involves reduced activation of effector T cells, potentiation of Treg cells, and enhanced expression of the PD-1 costimulatory pathway.

Estrogen (E2)-induced immunomodulation involves dual effects on antigen-presenting cells (APC) and CD4(+)CD25(+) regulatory T cells (Treg) but not a direct effect on effector T cells. In this report, we further investigated the effects of E2 on APC and Treg function. We found that E2 treatment in vivo strongly reduced recovery of APC from the peritoneal cavity and inhibited induction of the inflammatory cytokines interleukin (IL)-12 and interferon-gamma but enhanced secretion of IL-10. Moreover, E2-conditioned bone marrow-derived dendritic cells (BM-DC) could both enhance Treg activity and directly inhibit responder T cells in the absence of Treg cells. We examined whether this E2-induced inhibitory activity of BM-DC might involve costimulation through the recently described PD-1 pathway. Both E2 and pregnancy markedly enhanced PD-1 expression in several types of APC, including macrophages, B cells, and especially dendritic cells (DC). Similarly to E2-induced enhancement of FoxP3 expression and experimental autoimmune encephalomyelitis protection, E2-induced enhancement of PD-1(+) cells was also mediated through estrogen receptor alpha (Esr1) in DC and macrophages but not in B cells. Based on antibody inhibition studies, PD-1 interaction with its ligands, PDL-1 and especially PDL-2, could mediate either positive or negative regulatory signaling in both mature and immature E2-conditioned DC, depending, respectively, on a relatively high (10:1) or low (1:1) ratio of T cells:BM-DC. These novel findings indicate that E2-induced immunomodulation is mediated in part through potentiation in BM-DC of the PD-1 costimulatory pathway.

Animals↗
PubMed2002

Improved intestinal transport of PD 158473, an N-methyl-D-aspartate (NMDA) antagonist, by involvement of multiple transporters.

The objective of this research was to determine the characteristics of intestinal transport of PD 0158473 using in vitro Caco-2 cells as well as in situ single-pass rat intestinal perfusion models. Because apical (AP)-to-basolateral (BL) transport was greater (1.8- fold) than BL-to-AP transport in the Caco-2 cell model, identification of carrier system(s) involved was further investigated. Cellular uptake of PD 0158473 was concentration and/or pH dependent and significantly inhibited by substrates of dipeptide and monocarboxylic acid transporters. Although this compound is an analog of L-Phe and previous studies demonstrated a high affinity of this compound to large neutral amino acid transporter, the involvement of amino acid carriers did not appear to be significant in the Caco-2 cell model. Subsequently, in situ single-pass intestinal perfusion studies in rats demonstrated that intestinal absorption of PD 0158473 was not concentration dependent at a concentration range tested but significantly inhibited by various dipeptides as well as substrates of dipeptide transporters. The difference in the concentration-dependent transport of PD 0158473 between Caco-2 cells and the rat perfusion model could be explained by the difference in the affinity (apparent K(m)) of PD 0158473 between Caco-2 cells (107 microM) and rat tissue (>1 mM). The present study suggested that multiple transporters are involved in the transcellular transport of this amino-acid analogue compound, of which peptide transporters could play a major role.

Animals↗
PubMed2006

Regional brain volumes distinguish PSP, MSA-P, and PD: MRI-based clinico-radiological correlations.

Progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) are neurodegenerative disorders, each with a prevalence of around 5 per 100,000. Regional brain atrophy patterns differ in the two disorders, however, and magnetic resonance imaging is sometimes helpful in distinguishing them in the later stages. We measured whole brain and regional volumes, including cerebellum, pons, midbrain, superior cerebellar peduncle (SCP), and ventricular volumes as well as frontal and posterior-inferior cerebral regions in 18 subjects with PSP, 9 with MSA-P (parkinsonian phenotype), 9 with Parkinson's disease (PD), and 18 healthy controls. Associations between these volumes, cognitive profiles, and clinical measures of disease severity and motor disability were assessed. Mean midbrain volume was 30% smaller in PSP than in PD or controls (P < 0.001) and 15% smaller than in MSA-P (P = 0.009). The mean SCP volume in PSP was 30% smaller than in MSA-P, PD, or controls (P < 0.001). Mean cerebellar volumes in MSA-P were 20% smaller than in controls and PD and 18% smaller than in PSP (P = 0.01). Mean pontine volume in MSA-P was 30% smaller than in PD or controls (P < 0.001) and 25% smaller than in PSP (P = 0.01). Motor disability was most strongly associated with midbrain volume, and more severe executive dysfunction was associated with reduced frontal volume. These distinct patterns of cortical and subcortical atrophy, when considered together rather than independently, better differentiate PSP and MSA-P from each other and also from healthy controls.

Aged↗
PubMed1997

Molecular cloning and chromosomal localization of PD-Ibeta (PDNP3), a new member of the human phosphodiesterase I genes.

Phosphodiesterase I (EC 3.1.4.1)/nucleotide pyrophosphatase (EC 3.6.1.9) enzymes are a family of type II transmembrane proteins that catalyze the cleavage of phosphodiester and phosphosulfate bonds of a variety of molecules, including deoxynucleotides, NAD, and nucleotide sugars. The human genes for two members of this family have been cloned and designated PC-1 (PDNP1) and PD-Ialpha/autotaxin (PDNP2). We have now cloned the third member of this family from a human prostate cDNA library and designated it human phosphodiesterase-Ibeta (PD-Ibeta). The PD-Ibeta cDNA contains a 2625-bp-long open reading frame which encodes an 875-amino-acid protein. COS-7 cells transfected with an expression vector, pBK-CMV, containing PD-Ibeta cDNA had high phosphodiesterase I activity compared to the mock-transfected cells. By using in situ hybridization to human metaphase chromosomes, we have assigned the locus for the PD-Ibeta (PDNP3) gene to the q22 region of human chromosome 6.

Amino Acid Sequence↗
PubMedDate not supplied

Pharmacological characteristics of endothelin receptors in the rabbit ventricular myocardium: the nonselective endothelin receptor antagonist PD 145065 antagonizes the positive inotropic effect of endothelin-3 but not of endothelin-1.

Endothelin-3 (ET-3) elicited a concentration-dependent positive inotropic effect on rabbit papillary muscle, the maximal response being approximately 65% of the maximal response to isoproterenol. ET-1 induced a positive inotropic effect over the concentration range below 10(-9) M, at which ET-3 did not produce a positive inotropic effect, but the maximal response to ET-1 was equivalent to or slightly lower than that of ET-3. The nonselective ET receptor antagonist PD 145065 effectively antagonized the positive inotropic effect of ET-3 in a concentration-dependent manner and abolished it at 10(-5) M. PD 145065 decreased the positive inotropic effect induced by ET1 at lower concentrations (< 10(-9) M) but it did not affect the main portion of the concentration-response curve for the positive inotropic effect, i.e., the effect induced by high concentrations (> 10(-9) M) of ET-1. PD 145065 antagonized also the positive inotropic effect of sarafotoxin S6c. PD 145065 inhibited the specific binding of [125I]ET-1 and of [125I]ET-3 with a high- and a low-affinity site for competition. ETB selective ligands, RES-701-1 and sarafotoxin S6c, displaced [125Iuc]ET-3 with high affinity but they scarcely affected the [125I]ET-1 binding. These findings indicate that different subtypes of the ET receptor are responsible for the induction of the positive inotropic effect of ET-3 and ET-1. ET receptors involved in the production of the positive inotropic effect in the rabbit ventricular myocardium have pharmacological characteristics that are different from those of conventional ET receptors originally classified based on the pharmacological findings in noncardiac tissues. The positive inotropic effect of ET-3 in the rabbit ventricular muscle may be mediated predominantly by ETA1 receptors that are susceptible to PD 145065 as well as BQ-123 and FR139317, and partially mediated by ETB receptors that are inhibitable with RES-701-1. ETA2 receptors that are resistant to ETA selective as well as nonselective antagonists may mainly be responsible for the positive inotropic effect of ET-1 in the rabbit ventricular muscle.

Animals↗
PubMed1989

In vitro activity of PD 117596-2, a broad-spectrum difluoroquinolone.

The activity of PD 117596-2, a novel quinolone, was compared to that of other quinolones, ceftazidime, imipenem and gentamicin. PD 117596-2 inhibited most Enterobacteriaceae at concentrations less than 0.25 micrograms/ml, being equal or superior in activity to ciprofloxacin and 2- to 4-fold more active than ofloxacin. It inhibited ceftazidime-resistant Enterobacter spp., Citrobacter spp. and Serratia marcescens. The MIC90 for Pseudomonas aeruginosa, including strains with imipenem MICs of 8 micrograms/ml and gentamicin MICs greater than 16 micrograms/ml, was 0.25 micrograms/ml. PD 117596-2 was more active than ciprofloxacin against Pseudomonas cepacia and Pseudomonas maltophilia, and it inhibited Neisseria gonorrhoeae and Haemophilus influenzae at less than 0.03 micrograms/ml. PD 117596-2 inhibited staphylococci at 0.5 micrograms/ml, being 2-fold superior to other quinolones, and with an MIC of 0.25 micrograms/ml was more active against group A, B, C and G streptococci and Streptococcus pneumoniae. MICs for Bacteroides spp. were 2 micrograms/ml compared to 8-32 micrograms/ml for other agents. The frequency of spontaneous resistance was low (less than 10(-10]. Differences in MICs and MBCs were within one dilution, and there was a minimal effect of inoculum size. Although PD 117596-2 was less active at pH 5.5, MICs were less than 0.5 micrograms/ml.

Anti-Infective Agents↗
PubMed1991

Functional activity of the adenosine binding enhancer, PD 81,723, in the in vitro hippocampal slice.

The adenosine receptor binding enhancer, PD 81,723, enhances the inhibitory effects of exogenously applied adenosine in a dose-dependent manner in hippocampal brain slices. Extracellular recordings were obtained from the CA1 cell layer while electrically stimulating the stratum radiatum. Application of 1, 10 or 32 microM PD 81,723 in the presence of adenosine resulted in a dose-dependent reduction in the amplitude of the population spike which could be partially reversed by theophylline. In addition, hippocampal slices exposed to adenosine showed greater paired-pulse facilitation compared to control and this facilitation was significantly enhanced by the presence of PD 81,723. PD 81,723 had no effect when administered alone, but required the presence of adenosine. These results demonstrate that in addition to enhancing adenosine receptor binding, PD 81,723 also enhances the functional activity of adenosine in the hippocampal slice.

Adenosine↗
PubMed1996

Modulation of the in vivo actions of morphine by the mixed CCKA/B receptor antagonist PD 142898.

The ability of a mixed CCKA/B receptor antagonist PD 142898 (benzenebutanic acid, beta-[[3-(1 H-indol-3-yl)-2-methyl-2-[[[(2-methyl- cyclohexyl)oxy]carbonyl]amino]-1-oxopropyl]amino]-[1 S-[1 alpha [S*(R*)]-2 beta]]) to modulate the antinociceptive, positive reinforcing and gastrointestinal actions of morphine was investigated in the rat. PD 142898 antagonised the development and maintenance of morphine (2.0 mg/kg, s.c.) induced conditioned place preference at 0.1 mg/kg, i.p. However, it potentiated the antinociceptive action of a subthreshold dose of morphine in the radiant tail flick model at doses of 0.001 and 0.01 mg/kg, s.c. Furthermore, PD 142898 (0.0001-1.0 mg/kg, s.c.) also potentiated the antinociceptive action of morphine (1.0 mg/kg, s.c.) against the late phase of formalin response associated with inflammation at the dose of 0.001-1.0 mg/kg. PD 142898 (0.001 mg/kg, s.c.) blocked the development of tolerance to morphine in the formalin test. It failed (0.001-1.0 mg/kg, i.p.) to modulate the inhibitory action of morphine (5.0 mg/kg, s.c.) on gastrointestinal transit as measured using the charcoal meal test. It is argued that the effect of PD 142898 in the conditioned place preference test involves antagonism of CCKA receptors, whilst the potentiation of the antinociceptive action of morphine is mediated via blockade of CCKB receptors. These results suggest that the mixed CCKA/B receptor antagonist may potentiate the analgesic action of morphine, block the development of tolerance without a concomitant increase in constipation and may also reduce the abuse potential of the opiate.

Animals↗
PubMed1988

The effects of the kappa agonist PD-117302 on feeding behaviour in obese and lean Zucker rats.

It has been suggested that super-sensitivity to, or overactivity of, endogenous opioid systems, particularly the dynorphin system, may be important in the development of obesity in the obese mouse (ob/ob). We have investigated the possibility that an increase in sensitivity to kappa agonists may also play a role in the development of obesity in another mutant rodent, the Zucker rat. The effects of the selective kappa agonist PD-117302 were investigated in both lean and obese Zucker rats. The lean animals appeared to be more sensitive to the initial hyperphagic effects of PD-117302 than their obese littermates, although this initial hyperphagia was followed by a subsequent decrease in food intake so that by the end of the six-hour test period the animals treated with PD-117302 had eaten less than the saline-treated controls. These changes in food intake were paralleled by increases and decreases in the duration of time spent feeding throughout the experiment. At the doses used in this study PD-117302 had no effect on locomotor activity. It is concluded that obese Zucker rats are not more sensitive to the hyperphagic effects of the kappa agonist (PD-117302 than their lean littermates and therefore it seems unlikely that increased sensitivity to an endogenous kappa opioid system plays a major part in the overeating and obesity observed in this strain of rat.

Animals↗
PubMed1992

Permanent implants using Au-198, Pd-103 and I-125: radiobiological considerations based on the linear quadratic model.

Based on the linear-quadratic model, we perform calculations to compare the possible radiobiologic results achieved with permanent implants using Au-198, Pd-103, and I-125. We examine the influence of the radiobiophysical parameters (i.e. alpha, beta, SLD repair kinetics, tumor doubling time (Tp), tumor growth delay, and prescribed dose) on the calculated radiobiologic indices or endpoints. The radiobiologic indices or endpoints include the effective treatment time (Teff) (beyond which the additional dose delivered is wasted), the biologically effective dose (BED), and cell surviving fractions. Within the range of reported values of the various parameters, Tp is the most significant in affecting Teff, BED, and the degree of cell inactivation. The effect of Tp and Teff and BED is larger for isotopes with longer half-lives, for which the rate of tumor regrowth is more important. For Tp of 5 to 30 days, the Teff are 14 to 21 days for Au-198, 58 to 102 days for Pd-103, and 120 to 275 days for I-125. For this range of Tp, the wasted doses are less than 5% for Au-198, 15 to 3% for Pd-103, and 30 to 5% for I-125. For reference prescription doses of 60, 120, and 160 Gy for implants using Au-198, Pd-103, and I-125, respectively, the BED and the associated cell-kill is the lowest for Au-198, whereas Pd-103 and I-125 implants are more effective for fast-growth (Tp less than 10 days) and slow-growth (Tp greater than 10 days) tumors, respectively.

Brachytherapy↗
PubMed2004

PD-1 inhibits T-cell receptor induced phosphorylation of the ZAP70/CD3zeta signalosome and downstream signaling to PKCtheta.

Engagement of the immunoinhibitory receptor, programmed death-1 (PD-1) attenuates T-cell receptor (TCR)-mediated activation of IL-2 production and T-cell proliferation. Here, we demonstrate that PD-1 modulation of T-cell function involves inhibition of TCR-mediated phosphorylation of ZAP70 and association with CD3zeta. In addition, PD-1 signaling attenuates PKCtheta activation loop phosphorylation in a cognate TCR signal. PKCtheta has been shown to be required for T-cell IL-2 production. A phosphorylated PD-1 peptide, corresponding to the C-terminal immunoreceptor tyrosine-switch motif (ITSM), acts as a docking site in vitro for both SHP-2 and SHP-1, while the phosphorylated peptide containing the N-terminal PD-1 immunoreceptor tyrosine based inhibitory motif (ITIM) associates only with SHP-2.

Amino Acid Sequence↗