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Strontium doped lanthanum manganite (LSM) powders were synthesized by three different routes: azeotropic distillation, sol-gel and solid state reaction respectively. The LSM samples, made by azeotropic distillation and sol-gel methods were prepared by firing at 1000 °C for 6 h, and the LSM sample, made by solid state reaction method was produced by sintering at 1400 °C for 18 h. The samples were characterized by XRD, TEC, SEM, EIS and polarization performance analysis. The results show that all the samples made by different methods have pure orthorhombic LSM phase, however exhibit different micro structure and electrochemical characterization, which relates to the different synthesis methods. The solid state reaction method produces the samples with larger particle size compared with azeotropic distillation and sol-gel methods. The powders made by azeotropic distillation method have less agglomerated particles compared with that made by sol-gel method because the precursor in the former is dispersed in n-butanol before sintering. The polarization current density of powder made by azeotropic distillation method was twice of that made by sol-gel method and four times of that made by solid state reaction method. The values of polarization resistance ( R p ) are 0.35 Ω · cm 2 for the cathode synthesized by azeotropic distillation route, which is much lower than sol-gel (1.5 Ω · cm 2 ) and solid state reaction (2.3 Ω · cm 2 ) at 800 °C.

Objective Increased nucleoside triphosphate pyrophosphohydrolase (NTPPPH) activity in chondrocytes is associated with cartilage matrix inorganic pyrophosphate (PPi) supersaturation in chondrocalcinosis. This study compared the roles of the transforming growth factor β (TGFβ)–inducible plasma cell membrane glycoprotein-1 (PC-1) and the closely related B10 NTPPPH activities in chondrocyte PPi metabolism. Methods NTPPPH expression was studied using reverse transcriptase–polymerase chain reaction and Western blotting. Transmembrane PC-1 (tmPC-1), water-soluble secretory PC-1 (secPC-1), and transmembrane B10 were expressed by adenoviral gene transfer or plasmid transfection, and expression of PPi was assessed in cultured articular chondrocytes and immortalized NTPPPH-deficient costal chondrocytes (TC28 cells). Results PC-1 and B10 messenger RNA were demonstrated in articular cartilages in situ, in untreated cultured normal articular chondrocytes, and in TC28 cells. Expression of tmPC-1 and secPC-1, but not B10, rendered the NTPPPH-deficient TC28 cells able to increase expression of extracellular PPi, with or without addition of TGFβ (10 ng/ml) to the media. More plasma membrane NTPPPH activity was detected in cells transfected with tmPC-1 than in cells transfected with B10. Furthermore, confocal microscopy with immunofluorescent staining of articular chondrocytes confirmed preferential plasma membrane localization of PC-1, relative to B10. Finally, both PC-1 and B10 increased the levels of intracellular PPi, but PC-1 and B10 appeared to act principally in different intracellular compartments (Golgi and post-Golgi versus pre-Golgi, respectively). Conclusion PC-1 and B10 NTPPPH activities were not redundant in chondrocytes. Although increased PC-1 and B10 expression caused elevations in intracellular PPi, the major effects of PC-1 and B10 were exerted in distinct subcellular compartments. Moreover, PC-1 (transmembrane and secreted), but not B10, increased the levels of extracellular PPi. Differential expression of PC-1 and B10 could modulate cartilage mineralization in degenerative joint diseases.

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.

PDNP (phosphodiesterase I/nucleotide pyrophosphatase) is one of a series of ectoenzymes that are involved in hydrolysis of extracellular nucleotides. PDNP possesses ATPase (EC 3.6.1.3) and ATP pyrophosphatase (EC 3.6.1.8) activities. Mammalian PDNP consists of three closely related family proteins (PDNP1, -2, and -3), and they are expressed in different cell types and at different developmental stages. Rat PDNP3 is expressed in a subset of immature glial cells and in the alimentary tract. Human PDNP3 is expressed in glioma cells, prostate, and uterus, but not in the alimentary tract. We have cloned genomic DNA containing the whole coding region of the human PDNP3 gene and determined its exon–intron structure. The human PDNP3 gene spans over 60 kb and is organized into 25 exons and 24 introns. We determined the nucleotide sequence of the 5′-flanking region of human and rat PDNP3 genes. The upstream region of both species lacks a canonical TATA box and contains a putative binding site for CCAAT enhancer-binding proteins near the transcription start site. Promoter activity analysis of the 5′-flanking region revealed that the sequence around the CCAAT box is required for its transcriptional activity in 9L rat glioma cells. A gel shift assay demonstrated that 9L nuclear extract contains proteins that bind to this region.

Objectives Through studying the NK cell activity, the pathological changes of myocardial cells and the changes of apoptosis in the process of recombinant interleukin -12 treat the mice with viral myocarditis, to explore the therapeutic effect and mechanism of apoptosis in the process of recombinant interleukin -12 treat the viral diseases, to further reveal the treatment effect and therapeutic mechanism of recombinant interleukin-12 to viral diseases, and to make a theoretical foundation for the clinical use of recombinant interleukin -12. Methods A total of 90 BALB/C inbreeding male mice weight 14–18 g were randomly divided into six groups, each group has 15 mice. They are blank control group, the virus control group, drug control group, rmIL-12 small dose treatment group, medium dose treatment group, high dose treatment group. Each mouse was injected Coxsackie B3 0.2 ml/d for three consecutive days by intraperitoneal injection, in addition to except the mouse in blank control group. After inoculating 4 h, in the blank control group and the virus control group, each mouse was inoculated 0.9% saline 0.1 ml / d by intraperitoneal injection, in the drug control group, each mouse was inoculated interferon-of γ 400 IU/d, rmIL-12 small-dose, medium-dose and high-dose treatment group, the mouse in each group were injected recombinant interleukin-12 respectively 1 ng/d, 10 ng/d, 100 ng/d for five consecutive days. The time of injecting virus is the zeroth day. At the fifth day, we take 10 mice from each group, than killed them by cervical dislocation. We removed the spleens for testing the NK cell activity, under sterile conditions. We removed the hearts, than make heart specimens. We soaked the heart in 10% formalin solution and marked them for the test of heart pathology and apoptosis. NK cell activity was measured by MTT assay. Apoptosis was detected by TUNEL and pathological scores. Cardiac muscle pathology was detected by HE staining. The statistical data was expressed as mean±SD (□±S), The data were analysed by SPSS17.0 statistical software analysis system. Groups were analysed using analysis of variance. p Results In addition to the blank control group, each group can be detected the apoptosis of myocardial cells. The pathological scores of apoptotic cells are that, high dose treatment group is 29.18%, medium dose treatment group is 20.97%, small dose treatment group is 12.03%, drug control group is 10.51%, virus control group is 15.63%. The largest number of apoptotic cells is the high dose treatment group, followed by the middle dose treatment group, and the low dose treatment group and the virus control group is less than the above two groups. The NK cell activity in each group is that, blank control group is 29.58±4.56%, virus control group is 46.99±6.31%, drug control group is 34.54±3.98%, small dose treatment group is 42.14±4.02%, medium dose treatment group is 54.55±7.17%, high dose treatment group 57.06±4.55%. There are statistically significant differences in different groups about NK cell activity, F=34.98, p Conclusions In middle-dose treatment group, the number of myocardial cell degeneration and necrosis is least, indicating recombinant interleukin −12 have therapeutic action to viral myocarditis. The number of apoptotic myocardial cells increased with therapeutic dose of recombinant interleukin −12, and moderate apoptosis have an active role to clear virus-infected cells. Which indicating apoptosis is one of the treatment mechanism of recombinant interleukin-12.