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PubMed2003

Disorder and suppression of quantum confinement effects in Pd nanoparticles.

Size-selectable ligand-passivated crystalline and amorphous Pd nanoparticles (<4 nm) are synthesized by a novel two-phase process and verified by high-resolution transmission electron microscopy. Scanning tunneling spectroscopy preformed at 5 K on these two types of nanoparticles exhibits clear Coulomb blockade and Coulomb staircases. Size dependent multipeak spectral features in the differential conductance curve are observed for the crystalline Pd particles but not for the amorphous particles. Theoretical analysis shows that these spectral features are related to the quantized electronic states in the crystalline Pd particle. The suppression of the quantum confinement effect in the amorphous particle arises from the reduction of the degeneracy of the eigenstates and the level broadening due to the reduced lifetime of the electronic states.

Journal Article↗
PubMed1981

Tolerability of ibuprofen and flurbiprofen in G-6-PD deficient subjects: in vitro study.

1 A 'GSH (reduced glutathione) stability test' which consists of incubating blood samples with acetylphenylhydrazine and other test drugs and measuring GSH level before and after incubation, was carried out. 2 Application of this test to the blood of eight normal volunteers and twelve known G-6-PD deficient persons demonstrated that acetylphenylhydrazine and primaquine produced a significant decrease in GSH levels in G-6-PD deficient red cells compared to the reduction seen in normal red cells incubated with these drugs. No such change was observed with aspirin, ibuprofen and flurbiprofen. 3 The results of this in vitro study seem to indicate that ibuprofen and flurbiprofen are relatively innocuous in G-6-PD deficient individuals.

Erythrocytes↗
PubMed2002

Experimental determination of dosimetric characterization of a newly designed encapsulated interstitial brachytherapy source of 103Pd-model Pd-1.

A newly designed encapsulated 103Pd source has been introduced (BrachySeed-Pd-103, also named Model Pd-1, manufactured by DRAXIMAGE Inc. and distributed by Cytogen Corp.) for interstitial brachytherapy to provide more isotropic dose distributions. In this work, the dosimetric characteristics of the 103Pd source were measured with micro LiF TLD chips and dosimetry parameters were characterized based upon the American Association of Physicists in Medicine (AAPM) Task Group No. 43 formalism. The dose rate constant of the sources was determined to be 0.66 +/-0.05 cGy h(-1) U(-1). The radial dose function was measured and was found to be similar to that of the Theragenics Model 200 103Pd source. The anisotropy constant for the Model Pd-1 source was determined to be 1.03.

Anisotropy↗
PubMed2001

Autoimmune dilated cardiomyopathy in PD-1 receptor-deficient mice.

Dilated cardiomyopathy is a severe pathology of the heart with poorly understood etiology. Disruption of the gene encoding the negative immunoregulatory receptor PD-1 in BALB/c mice, but not in BALB/c RAG-2-/- mice, caused dilated cardiomyopathy with severely impaired contraction and sudden death by congestive heart failure. Affected hearts showed diffuse deposition of immunoglobulin G (IgG) on the surface of cardiomyocytes. All of the affected PD-1-/- mice exhibited high-titer circulating IgG autoantibodies reactive to a 33-kilodalton protein expressed specifically on the surface of cardiomyocytes. These results indicate that PD-1 may be an important factor contributing to the prevention of autoimmune diseases.

Animals↗
PubMed1991

In vitro antibacterial activities of PD 131628, a new 1,8-naphthyridine anti-infective agent.

PD 131628 is a new aminopyrrolidine-substituted fluorocyclopropyl naphthyridine quinolone which possesses high in vitro activity against a wide spectrum of bacterial species. The MICs for greater than or equal to 90% of strains were 0.125 to 0.25 microgram/ml for staphylococci, Streptococcus pyogenes, and S. pneumoniae; 0.5 micrograms/ml for S. agalactiae and Enterococcus faecalis; 0.125 micrograms/ml for members of the family Enterobacteriaceae and Acinetobacter spp.; 0.5 micrograms/ml for Pseudomonas aeruginosa; and less than or equal to 0.03 micrograms/ml for Haemophilus influenzae, Moraxella (Branhamella) catarrhalis, and Neisseria gonorrhoeae. In these in vitro comparisons with ciprofloxacin, PD 131628 is more active against gram-positive organisms, approximately equivalent against gram-negative organisms, and, like most other quinolones, relatively inactive against gram-negative anaerobes. In most instances, the in vitro potency of PD 131628 exceeded those of widely used compounds: ciprofloxacin, imipenem, ampicillin, penicillin G, oxacillin, cefazolin, ceftazidime, cefoxitin, cefsulodin, aztreonam, piperacillin, amikacin, spectinomycin, doxycycline, erythromycin, metronidazole, and vancomycin.

Anti-Bacterial Agents↗
PubMed2016

Immunodominant Dengue Virus-Specific CD8+ T Cell Responses Are Associated with a Memory PD-1+ Phenotype.

UNLABELLED: Dengue disease is a large public health problem that mainly afflicts tropical and subtropical regions. Understanding of the correlates of protection against dengue virus (DENV) is poor and hinders the development of a successful human vaccine. The present study aims to define DENV-specific CD8(+)T cell responses in general and those of HLA alleles associated with dominant responses in particular. In human blood donors in Nicaragua, we observed a striking dominance of HLA B-restricted responses in general and of the allele B*35:01 in particular. Comparing these patterns to those in the general population of Sri Lanka, we found a strong correlation between restriction of the HLA allele and the breadth and magnitude of CD8(+)T cell responses, suggesting that HLA genes profoundly influence the nature of responses. The majority of gamma interferon (IFN-&#x3b3;) responses were associated with effector memory phenotypes, which were also detected in non-B*35:01-expressing T cells. However, only the B*35:01 DENV-specific T cells were associated with marked expression of the programmed death 1 protein (PD-1). These cells did not coexpress other inhibitory receptors and were able to proliferate in response to DENV-specific stimulation. Thus, the expression of particular HLA class I alleles is a defining characteristic influencing the magnitude and breadth of CD8 responses, and a distinct, highly differentiated phenotype is specifically associated with dominant CD8(+)T cells. These results are of relevance for both vaccine design and the identification of robust correlates of protection in natural immunity. IMPORTANCE: Dengue is an increasingly significant public health problem as its mosquito vectors spread over greater areas; no vaccines against the virus have yet been approved. An important step toward vaccine development is defining protective immune responses; toward that end, we here characterize the phenotype of the immunodominant T cell responses. These DENV-reactive T cells express high levels of the receptor programmed death 1 protein (PD-1), while those from disease-susceptible alleles do not. Not only does this represent a possible correlate of immunodominance, but it raises the hypothesis that PD-1 might be a regulator that prevents excessive damage while preserving antiviral function. Further, as this study employs distinct populations (Nicaraguan and Sri Lankan donors), we also confirmed that this pattern holds despite geographic and ethnic differences. This finding indicates that HLA type is the major determinant in shaping T cell responses.

Alleles↗
PubMed1999

Lymphocyte activation during acute simian/human immunodeficiency virus SHIV(89.6PD) infection in macaques.

Host-virus interactions control disease progression in human immunodeficiency virus-infected human beings and in nonhuman primates infected with simian or simian/human immunodeficiency viruses (SHIV). These interactions evolve rapidly during acute infection and are key to the mechanisms of viral persistence and AIDS. SHIV(89.6PD) infection in rhesus macaques can deplete CD4(+) T cells from the peripheral blood, spleen, and lymph nodes within 2 weeks after exposure and is a model for virulent, acute infection. Lymphocytes isolated from blood and tissues during the interval of acute SHIV(89.6PD) infection have lost the capacity to proliferate in response to phytohemagglutinin (PHA). T-cell unresponsiveness to mitogen occurred within 1 week after mucosal inoculation yet prior to massive CD4(+) T-cell depletion and extensive virus dissemination. The lack of mitogen response was due to apoptosis in vitro, and increased activation marker expression on circulating T cells in vivo coincided with the appearance of PHA-induced apoptosis in vitro. Inappropriately high immune stimulation associated with rapid loss of mature CD4(+) T cells suggested that activation-induced cell death is a mechanism for helper T-cell depletion in the brief period before widespread virus dissemination. Elevated levels of lymphocyte activation likely enhance SHIV(89.6PD) replication, thus increasing the loss of CD4(+) T cells and diminishing the levels of virus-specific immunity that remain after acute infection. The level of surviving immunity may dictate the capacity to control virus replication and disease progression. We describe this level of immune competence as the host set point to show its pivotal role in AIDS pathogenesis.

Animals↗
PubMed2004

PD-L1/B7H-1 inhibits the effector phase of tumor rejection by T cell receptor (TCR) transgenic CD8+ T cells.

Although increased circulating tumor antigen-specific CD8(+) T cells can be achieved by vaccination or adoptive transfer, tumor progression nonetheless often occurs through resistance to effector function. To develop a model for identifying mechanisms of resistance to antigen-specific CTLs, poorly immunogenic B16-F10 melanoma was transduced to express the K(b)-binding peptide SIYRYYGL as a green fluorescent protein fusion protein that should be recognized by high-affinity 2C TCR transgenic T cells. Although B16.SIY cells expressed high levels of antigen and were induced to express K(b) in response to IFN-gamma, they were poorly recognized by primed 2C/RAG2(-/-) T cells. A screen for candidate inhibitory ligands revealed elevated PD-L1/B7H-1 on IFN-gamma-treated B16-F10 cells and also on eight additional mouse tumors and seven human melanoma cell lines. Primed 2C/RAG2(-/-)/PD-1(-/-) T cells showed augmented cytokine production, proliferation, and cytolytic activity against tumor cells compared with wild-type 2C cells. This effect was reproduced with anti-PD-L1 antibody present during the effector phase but not during the priming culture. Adoptive transfer of 2C/RAG2(-/-)/PD-1(-/-) T cells in vivo caused tumor rejection under conditions in which wild-type 2C cells or CTLA-4-deficient 2C cells did not reject. Our results support interfering with PD-L1/PD-1 interactions to augment the effector function of tumor antigen-specific CD8(+) T cells in the tumor microenvironment.

Animals↗
PubMed2004

B7-H1 expression on non-small cell lung cancer cells and its relationship with tumor-infiltrating lymphocytes and their PD-1 expression.

PURPOSE: B7-H1/PD-L1 (B7-H1) and B7-DC/PD-L2 (B7-DC) are ligands for the receptor PD-1, which is known to negatively regulate T-cell activation. In the present study, we investigated the expression of B7-H1 and B7-DC in tumor specimens of non-small cell lung cancer and their relationships with clinicopathological variables and postoperative survival. Furthermore, we examined the correlation between B7-H1 expression on tumor cells and the number of tumor-infiltrating lymphocytes (TILs) or PD-1 expression on TILs. EXPERIMENTAL DESIGN: The expression of B7-H1 and B7-DC in 52 surgically resected specimens of non-small cell lung cancer was evaluated immunohistochemically. RESULTS: Expression of B7-H1 and B7-DC was focally observed in all non-small cell lung cancer tumor specimens. No relationship was found between the expression of B7-H1 or B7-DC and clinicopathological variables or postoperative survival. However, in the same sections evaluated, significantly fewer TILs were identified in B7-H1-positive tumor regions than in B7-H1-negative tumor regions in a subset of five patients (P = 0.01). Moreover, the percentage of TILs expressing PD-1 was significantly lower in B7-H1-positive tumor regions than in B7-H1-negative tumor regions (P = 0.02). CONCLUSIONS: The expression of B7-H1 on tumor cells in local areas reciprocally correlated with the number of TILs, and this may contribute to negative regulation in antitumor immune responses in non-small cell lung cancer.

Adult↗
PubMed2005

Intraperitoneal heparin ameliorates the systemic inflammatory response in PD patients.

BACKGROUND: Patients with end-stage renal disease (ESRD) suffer from high mortality rates of cardiovascular diseases, conditions closely linked to the magnitude of their chronic low-grade inflammation. As heparins have been suggested to possess anti-inflammatory properties, we set out to investigate the impact of long-term treatment with intraperitoneal heparin on local and systemic inflammation in peritoneal dialysis (PD) patients. METHODS: In a double-blinded cross-over study, 21 PD patients with ESRD were randomised to inject either 4,500 anti-Xa IU tinzaparin or placebo (isotonic saline) into their morning dialysis bags every day for two periods of 3 months separated by a 1-month wash-out period. Blood and dialysate samples were analysed for inflammatory markers at the start and end of each treatment period. In dialysate, the appearance rates of the inflammatory markers were calculated to adjust for ultrafiltration variations. RESULTS: Eleven patients completed the trial. Treatment with intraperitoneal tinzaparin was accompanied with a median 25.8% reduction of the plasma C-reactive protein concentration (p = 0.032), a 7.3% reduction of the plasma fibrinogen concentration (p = 0.042) and a 54.5% reduction of the dialysate interleukin 6 appearance rate (p = 0.007) compared with placebo. CONCLUSION: Long-term treatment with intraperitoneal tinzaparin of ESRD patients on PD reduces local and systemic concentrations of inflammatory markers.

Adult↗
PubMed1981

Haemoglobin variants, beta-thalassaemia and G-6-PD types in Liberia.

Haemoglobin variants, beta-thalassaemia and glucose-6-phosphate dehydrogenase (G-6-PD) types were studied in 702 individuals from Buchanan, Liberia. In this population haemoglobins S and C, beta-thalassaemia and G-6-PD deficiency were found together. There was a considerable tribal variation. In the tribes of eastern Liberia the S- and C-genes were uncommon and the beta-thalassaemia gene was rather frequent, while in western Liberia the S- and C-genes were more frequent and beta-thalassaemia uncommon. In the central and northern parts the S- and beta-thalassaemia genes were found together in relatively high frequencies. The rate of malaria infection was found to be lower in individuals with the sickle cell and beta-thalassaemia traits than in individuals with haemoglobin AA, but the difference was not statistically significant. The frequency of the delta-chain gene B2 was 1.4% in the total material and there was no significant tribal variation for this gene. The frequency of G-6-PD deficiency estimated in males was 16%.

Adolescent↗
PubMedDate not supplied

In vitro investigation of the intraphagocytic bioactivities of ciprofloxacin and the new fluoroquinolone agents, clinafloxacin (CI-960) and PD 131628.

In this study the intraphagocytic bioactivities of the new fluoroquinolone antimicrobial agents clinafloxacin (CI-960) and PD 131628 (the active metabolite of CI-990) were investigated in vitro at final concentrations of 0.0005-0.5 microgram/ml using human neutrophils and the combination of a radiometric and a colony-counting method, which enabled us to distinguish between intracellular bacteriostatic and bactericidal mechanisms. Ciprofloxacin was included for comparison. Staphylococcus aureus (ATCC 25923) and Escherichia coli (ATCC 25922) were used as the test intraphagocytic microbial pathogens. Clinafloxacin (> or = 0.05 microgram/ml) displayed potent intraphagocytic bactericidal activity against S. aureus, while PD 131628 was merely bacteriostatic. Ciprofloxacin displayed relatively unimpressive bacteriostatic rather than bactericidal activity for S. aureus. Against E. coli, the intraphagocytic activity of clinafloxacin (0.001-0.005 microgram/ml and above) was superior to that of PD 131628 or ciprofloxacin, which were approximately equipotent. Clinafloxacin is a potent intraphagocytic bactericidal agent for both gram-positive and gram-negative bacteria.

Anti-Infective Agents↗
PubMedDate not supplied

Susceptibility of Brucella melitensis to the new fluoroquinolone PD 131628: comparison with other drugs.

The antibacterial activity of PD 131628 was determined by the broth dilution method against 105 clinical isolates of Brucella melitensis. Fifty-two and ninety-nine percent of the isolates were inhibited by 0.06 and 0.12 microgram/ml of this quinolone, respectively. One strain which was resistant to 8 other fluoroquinolones, with a minimum inhibitory concentration (MIC) of > 4.0 micrograms/ml, did not show cross-resistance and had an MIC of 2.0 micrograms/ml. Of the 9 fluoroquinolones tested, PD 131628 was most inhibitory followed by CI-960. All the strains were susceptible to conventional drugs like gentamicin, rifampicin, tetracycline and trimethoprim-sulfamethoxazole, with MICs ranging between 0.12 and 1.0 microgram/ml. PD 131628 did not exhibit in vitro synergy with any of the conventional drugs.

Anti-Bacterial Agents↗
PubMedDate not supplied

An in vitro investigation of the bioactivities of ciprofloxacin and the new fluoroquinolone agents clinafloxacin (CI-960) and PD 131628 against Mycobacterium tuberculosis in human macrophages.

In this study the intracellular bioactivity of ciprofloxacin and the new fluoroquinolone agents clinafloxacin (CI-960) and PD 131628 against Mycobacterium tuberculosis (H37Rv) was compared with rifampicin using human macrophages. Monocyte-derived macrophages were infected with M. tuberculosis in the presence of 10% autologous serum and treated with the antibiotics for 2 days, either immediately after infection or 3 days post-infection. The survival of the intracellular microorganisms was determined using the BACTEC tuberculosis system. Clinafloxacin, although not as active, compared favourably with rifampicin at concentrations ranging from 0.1 to 5 micrograms/ml in both systems, whereas PD 131628 performed reasonably well only when added directly after infection. However, ciprofloxacin was relatively unimpressive with intracellular bioactivity detected only with the highest concentration used (5 micrograms/ml). The ability of clinafloxacin, but not PD 131628, to inhibit mycobacteria after most of the organisms have escaped from the fused phagosomes emphasizes the importance of using a prolonged incubation time after infection when screening new antituberculosis drugs for intracellular bioactivity.

Anti-Infective Agents↗
PubMed1978

Salicylamide glucuronide formation in newborn babies with G-6-PD deficiency.

Salicylamide glucuronide formation has been studied in 23 newborn babies with erythrocyte G-6-PD deficiency and in 15 normal newborns on the first day of life. Glucuronide formation was significantly lower (p less than 0.001) in the former in comparison with the controls. In the newborns with G-6-PD deficiency who subsequently became hyperbilirubinemic an even lower mean glucuronide formation was observed (p less than 0.01) in respect to the non-jaundiced G-6-PD-deficient newborns.

Glucosephosphate Dehydrogenase Deficiency↗
PubMed1986

Tarnishing in vivo of Ag-Pd-Cu-Zn alloys.

Pre-polished specimens of four Ag-Pd-Cu-Zn alloys have been tested for tarnishing while embedded in full acrylic dentures for from six to eight months in vivo. The results have been compared with those from previous immersion tests using 2% Na2S solutions. In both types of tests, a multiphase alloy consisting of a Pd-Cu-Zn-rich compound in a Ag-rich matrix displayed less corrosion and tarnish resistance than did alloys with compositions similar to the Pd-Cu-Zn-rich compound or the Ag-rich matrix. It is suggested that the presence of local microgalvanic cells due to chemical inhomogeneities caused the observed susceptibility to tarnishing. Sulfur was detected by a microprobe in the tarnish layer developed in the oral cavity. The discoloration on this multiphase alloy covered the interdendritic areas with short distances between the chemical inhomogeneities. This microstructural location was somewhat different from the many dark spots created predominantly on Ag-rich areas during in vitro testing. This difference is most likely due to dissimilar conditions with regard to sulfide ion concentrations, the presence of protein films, and the length of exposure time.

Aged↗
PubMed1993

Morphogenesis of a zone-specific adrenocortical cytotoxicity in guinea pigs administered PD 132301-2, an inhibitor of acyl-CoA:cholesterol acyltransferase.

PD 132301-2, a novel inhibitor of acyl-CoA:cholesterol acyltransferase, is adrenotoxic to several laboratory animal species. Morphogenesis of a zona fasciculata-specific cytotoxicity was evaluated in male Hartley guinea pigs administered 100 mg/kg of PD 132301-2 for up to 7 days. Reversibility of adrenal effects was assessed after a 14-day drug withdrawal period (day 21). Serum cortisol concentrations were determined under basal conditions and after administration of adrenocorticotrophic hormone (ACTH) on days 1, 2, 4, 7, and 21. Isolated foci of cortical cell degeneration and necrosis were apparent in outer zona fasciculata by 2 hr and throughout the zona fasciculata at 6 hr. Early degenerative ultrastructural changes included aggregation of smooth endoplasmic reticulum (SER), variable condensation of mitochondrial matrices and swelling of cristae, partitioning of organelles, autophagosome formation, and disruption of lipid globules. Lesions progressed to locally extensive or diffuse zonal necrosis on days 1 and 2 and near complete ablation of zona fasciculata by day 4. Fasciculata cells remaining on day 4 had reduced numbers and increased size of lipid globules, increased lysosomes, and, occasionally, aggregates of SER and mitochondria. On day 7, SER proliferation and lipid depletion were apparent in remaining cells. ACTH responses were attenuated 24 hr after the first dose, and reduction in basal cortisol levels were seen by 24 hr after the second dose with both effects maximal on day 7. After a 14-day withdrawal period, ACTH responses and adrenal morphology returned to normal. It was concluded that PD 132301-2 induced rapid, reversible, zone-specific, morphologic, and functional adrenocortical effects. Furthermore, mitochondria and SER represented early subcellular targets of toxicity.

Adrenal Cortex Diseases↗
PubMed2005

Atorvastatin improves peritoneal sclerosis induced by hypertonic PD solution in rats.

BACKGROUND: Peritoneal sclerosis is a complication of peritoneal dialysis and results in ultrafiltration failure. It is related to chronic peritoneal injury due to dialysis solution content and recurrent peritonitis. Statins have anti-inflammatory properties which may be of value in modulating responses to injury. We evaluated the capacity of atorvastatin to modify peritoneal alterations secondary to hypertonic glucose. METHODS: Thirty-two non-uremic rats were divided into three groups: group I (Sham) rats received no treatment (n=11), group II received hypertonic (3.86%, 10 ml/day) PD solution (n=10) and group III received hypertonic PD solution (10 ml/day) plus 80 mg/L atorvastatin in drinking water (n=11). After four weeks, a one-hour peritoneal equilibration test (PET) was performed with 3.86% PD solution. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D 1 /D 0 glucose), ultrafiltration volume (UF), dialysate protein, TGF-beta 1 and VEGF levels were determined. RESULTS: Administration of atorvastatin resulted in preserved UF (4.9+/-0.8 vs 7.5+/-0.6 mL, p <0.01), protein loss (2.2+/-0.2 vs 2.1+/-0.1 g/L, p >0.05), and peritoneal thickness (53+/-3 vs 26+/-4 microm, p <0.01). D 1 /D 0 glucose was significantly reduced in the dextrose group (0.70+/-0.02 vs 0.56+/-0.04, p <0.01). Both higher levels of TGF-ss 1 (206+/-40 vs 474+/-120 pg/mL, p<0.05), and VEGF in dialysate effluent (4+/-0.4 vs 7.9+/-3 pg/mL, p>0.05), was determined in the dextrose group. CONCLUSION: Exposure to hypertonic glucose solution resulted in alterations in peritoneal transport manifested by a rapid dissipation of the glucose gradient and resultant impaired UF response. Administration of atorvastatin led to prevention of these alterations. We suggest that the anti-inflammatory properties of statins are useful in providing protection of the peritoneal membrane from the effects of hypertonic glucose.

Animals↗