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Members of the E74-like factor (ELF) subfamily are involved in the immune stress process of organisms by regulating immune responses and the development of immune-related cells. PmE74 of Penaeus monodon was characterized and functionally analyzed in this study. The full length of PmE74 was 3106 bp, with a 5'-UTR of 297 bp, and a 3'-UTR of 460 bp. The ORF (Open reading frame) was 2349 bp and encoded 782 amino acids. Domain analysis showed that PmE74 contains a typical Ets domain. Multiple sequence alignment and phylogenetic tree analysis showed that PmE74 clustered with Litopenaeus vannamei E74 and displayed significant similarity (98.98%). PmE74 was expressed in all tissues tested in P. monodon, with the highest levels of expression observed in the testis, intestine, and epidermis. Different pathogen stimulation studies have revealed that PmE74 expression varies in response to different pathogen stimuli. A 96-h acute low salt stress study revealed that PmE74 in the hepatopancreas was upregulated and downregulated in the salinity 17 group and considerably downregulated in the salinity 3 group, whereas PmE74 in gill tissue was considerably downregulated in both groups. Further, by knocking down PmE74 and learning the trends of its linkage genes PmAQP1, PmNKA, PmE75, PmFtz-f1, PmEcR, and PmRXR in response to low salt stress, it was further indicated that PmE74 could have a vital role in the regulation of low salt stress. The SNP test revealed that PmE74-In1-53 was significantly associated with low salt tolerance traits in P. monodon (P 0.05). The findings of this study can aid in the advancement of molecular marker-assisted breeding in P. monodon, as well as provide fundamental data and methodologies for further investigation of its low salt tolerance strains in P. monodon.

A novel TRY homolog was cloned in Penaeus monodon by RACE technology, named PmTry (GenBank: KP998480). The PmTry cDNA was 916 bp, which encodes 266 amino acids with a predicted molecular weight of 28.38 KDa and an isoelectric point of 4.58. Homologous analysis indicated that PmTry shared 42%~91% similarity with other species. The phylogenetic tree showed that PmTry was closely related to Fenneropenaeus chinensis. Tissue expression profiles showed that PmTry was highest expressed in the hepatopancreas and the lowest expressed in the eyestalk nerve. It was expressed in the whole growth stage of P. monodon, but the relative expression level of each stage was significantly different. In addition, PmTry-524 and PmTry-798 were particularly related to growth traits of P. monodon by genotype. The SNP markers may provide a basis for genetic selection and breed improvement studies in P. monodon.

Metapenaeus affinis is a crustacean with important commercial value in the fishery of the South China Sea. Overfishing has resulted in the decline of the wild population and germplasm degradation. However, there is little background knowledge about its gonadal development, and there is a lack of research on the development of this species. To better understand the molecular regulatory mechanisms during gonadal development, here, we performed RNA-Seq on immature and mature ovaries and compared their transcriptomic signatures. 126,930,488 and 122,677,356 clean sequencing reads were obtained from the Illumina sequencing platform, respectively. 394 differentially expressed genes (DEGs) were identified, of which 136 were up-regulated, and 258 were down-regulated. Further analysis revealed rich transcriptional sequences, which have homology with genes related to reproduction and development. Expression patterns of COX, GPX, E3s, PCNA, STPK, and other genes were changed during ovarian development. Validation by qRT-PCR demonstrated the reliability of RNA-Seq. This study has made a significant contribution to the currently available sequence data of M. affinis and provided reference data for the development of genetic and breeding work.

The present study aimed to examine the expression of hyperuricemia (HUA)-related factors in the body fluids of HUA patients and in renal tissues and body fluids of HUA mice to elucidate the underlying mechanism of HUA and provide theoretical basis for the diagnosis, prevention and treatment of this disease. A total of 51 HUA patients (HUA group), and 36 healthy subjects (control group) were included in the present study. The peripheral blood and urine were collected from all patients and healthy subjects. A total of 20 male Kunming mice were used to construct HUA model, and another 20 mice were used as controls. The kidney tissues, peripheral blood and urine were collected from all mice. ELISA was performed to determine the levels of interleukin-6 receptor (IL-6R) proteins in the serum and urine of human or mice, while western blotting was employed to determine the protein expression in the kidney tissues of mice. Quantitative real-time polymerase chain reaction was used to measure the expression of mRNA and miR-30b in all sample types. Dual luciferase reporter assay was performed to identify the direct interaction between 3'-untranslated region of IL-6R mRNA and miR-30b. The expression of IL-6R mRNA and protein was increased in serum and urine of HUA patients, while the expression of miR-30b was reduced in HUA patients when compared with healthy subjects. The contents of uric acid, urea nitrogen and creatinine in the blood of HUA mice model were significantly elevated. Similarly, the expression of IL-6R mRNA and protein was increased in kidney, serum and urine of HUA mice model, while the expression of miR-30b was reduced in kidney tissues, serum and urine of HUA mice model. Dual luciferase reporter assay showed that miR-30b was able to bind with 3'-UTR seed region of IL-6R mRNA to regulate its expression. These findings demonstrated that the expression of IL-6R in patients and mouse with HUA is elevated, which is related with the down-regulation of miR-30b. Therefore, miR-30b might participate in the pathological process of HUA by regulating IL-6R.

Procambarus clarkii is an important economic species in China, and exhibit heat and cold tolerance in the main culture regions. To understand the mechanisms, we analyzed the hepatopancreas transcriptome of P. clarkii treated at 10 °C, 25 °C, and 30 °C, then 2092 DEGs and 6929 DEGs were found in 30 °C stress group and 10 °C stress group, respectively. KEGG pathway enrichment results showed that immune pathway is the main stress pathway for 10 °C treatment and metabolic pathway is the main response pathway for 30 °C treatment, which implies low temperature stress induces the damage of the immune system and increases the susceptibility of bacteria while the body response to high temperature stress through metabolic adjustment. In addition, flow cytometry proved that both high and low temperature stress caused different degrees of apoptosis of hemocytes, and dynamic transcription heat map analysis also identified the differential expression of HSPs family genes and apoptosis pathway genes under different heat stresses. This indicates that preventing damaged protein misfolding and accelerating cell apoptosis are necessary mechanisms for P. clarkii to cope with high and low temperature stress. Our research has deepened our understanding of the complex molecular mechanisms of P. clarkii in response to acute temperature stress, and provided a potential strategy for aquatic animals to relieve environmental duress.

Qi-Bin Yang,1,2 Ling-Qin Li,1 Quan-Bo Zhang,2,3 Yong-Long He,1 Qing-Sheng Mi,2 Jing-Guo Zhou4 1Department of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 2Henry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, Detroit, MI, 48202, USA; 3Department of Gerontology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 4Department of Rheumatology and Immunology, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, Sichuan Province, People’s Republic of ChinaCorrespondence: Qing-Sheng MiHenry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, 1 Ford Place, Detroit, MI, 48202, USATel +1-313-876-1017Email qmi1@hfhs.orgJing-Guo ZhouDepartment of Rheumatology and Immunology, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, Sichuan Province, People’s Republic of ChinaTel +86-28-8301-6078Email jgzhou@cmc.edu.cnObjective: MicroRNAs were identified as master-switch molecules limiting acute inflammatory response. This study investigated the potential role of microRNA (miR)-223 in the mechanism of gout.Methods: Wild-type (WT) and miR-223 knock-out (KO) mice were used to evaluate the phenotypes of gout models. Inflammatory cytokines were measured in air pouch and peritoneal cavity lavage fluid. In addition to miR-223 level in gout patients, miR-223 and pro-inflammatory genes were examined in bone marrow-derived macrophages (BMDMs) from mice as well as peripheral blood mononuclear cells from healthy controls (HC) treated with monosodium urate (MSU) crystals in vitro.Results: MiR-223 was up-regulated in the early phase in BMDMs from WT mice after MSU challenge and decreased rapidly, and this was not observed in miR-223 KO mice in vitro. In addition, miR-223 was required for macrophages homeostasis. In comparison with WT mice in vivo, miR-223 deficiency exacerbated swelling index of MSU-induced inflammation in foot pad and ankle joint models. MiR-223 deficiency also markedly aggravated inflammatory cells infiltration and cytokines release including interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) in the air pouch and peritonitis models. In the in vitro experiments, miR-223 deficiency promoted the inflammatory response by targeting NLR family pyrin domain containing protein 3 (NLRP3). Besides, miR-223 level was down-regulated in gout patients and in HC exposed to MSU in vitro.Conclusion: MiR-223 was down-regulated in gout patients and miR-223 deficiency exacerbated inflammatory response in diverse murine models, suggesting that up-regulation of miR-223 could be a potential therapeutic strategy for alleviating gouty inflammation.Keywords: miR-223, gout, animal models, cytokines, monosodium urate

A 48 year-old Chinese woman suffering from polyarthritis, irregular fever and trichomadesis was admitted to the hospital. A diagnosis of systemic lupus erythematosus (SLE) was made based on polyarthritis, pancytopenia, reduced complement 3, multiple positive autoantibodies, a positive Coomb's test and protein in her urine. In addition, splenomegaly was detected during physical examination and confirmed by abdominal ultrasonography and magnetic resonance imaging, indicating that the patient had SLE and portal hypertension. Further negative investigations ruled out the possibility of cirrhosis. The patient was diagnosed with active SLE complicated by noncirrhotic portal hypertension (NCPH) without liver histopathology, due to the patient's refusal for liver biopsy. Portal vein diameter and splenomegaly decreased following treatment with methylprednisolone, hydroxychloroquine and metoprolol tartrate. To date, SLE complicated by NCPH has rarely been reported, as it is under-recognized clinically as well as pathologically. Here we describe a case of SLE complicated by NCPH and review the literature for its characteristics, which may contribute to improving the recognition of NCPH and reducing missed and delayed diagnosis of this disorder.

Gouty arthritis (GA) is the most common inflammatory and immune-associated disease, and its prevalence and incidence exhibit yearly increases. The aim of the present study was to analyse the expression profile variation of long non-coding RNAs (lncRNAs) in GA patients and to explore the role of lncRNAs in the pathogenesis of GA. The peripheral blood mononuclear cells of GA patients and of healthy controls (HCs) were used to detect for the differentially expressed lncRNAs by microarray. The functional annotations and classifications of the differentially expressed transcripts were predicted using Gene Ontology (GO) and pathway analysis. The results were then verified by reverse transcription-quantitative (RT-q)PCR. A total of 1,815 lncRNAs and 971 mRNAs with a >2-fold difference in the levels of expression in the GA patients compared with those in the HCs were identified. According to the GO functional enrichment analysis, the differentially expressed lncRNAs were accumulated in terms including protein binding, catalytic activity and molecular transducer activity. The pathways predicted to be involved were the tumor necrosis factor signaling pathway, osteoclast differentiation, NOD-like receptor signaling pathway and NF-κB signaling pathway. The expression of six lncRNAs was measured by RT-qPCR and the results were consistent with those of the microarrays. Among these lncRNAs, AJ227913 was the most differentially expressed lncRNA in GA patients vs. HCs. The expression of several lncRNAs was significantly changed in GA patients compared with that in HCs, which suggests that these lncRNAs with differential expression levels may have an important role in the development and progression of GA.

Gout is sterile joint inflammation triggered by the damaging effects of monosodium urate (MSU) crystals accumulation. Previous studies suggest transcription factor T-bet plays an important role in inflammatory arthritis. Notably, mice lacking T-bet markedly reduced joint inflammation of rheumatoid arthritis models, however, the involvement of T-bet in gouty inflammation has yet to be clarified. Here, we took advantage of T-bet knockout (KO) mice to investigate the role of T-bet in the pathogenesis of MSU-induced gout inflammation. T-bet KO and wild type (WT) mice were used for models of acute inflammation induced with MSU crystals, including footpad, air pouch and peritonitis models. Inflammatory cytokines and phagocytosis were detected in bone-marrow-derived macrophages (BMDMs) from T-bet KO and WT mice treated with MSU crystals in vitro. In addition, T-bet expression in peripheral blood mononuclear cells (PBMCs) from gout patients was measured, as well as plasma inflammatory cytokines. We found that the levels of interleukin (IL)-17, IL-23, and interferon-γ were reduced, but tumor necrosis factor-α was not, in BMDMs from T-bet KO compared with WT mice after MSU challenge in vitro, as well as MSU phagocytosis. In comparison with WT mice in vivo, the swelling index of T-bet KO mice was significantly decreased in the footpad model. T-bet deficiency also dramatically relieved MSU-induced inflammatory cell infiltration in peritonitis and air pouch models in vivo, and as well as the IL-1β levels of air pouch lavage fluid (APLF). In addition, plasma IL-17 and IL-23 levels were elevated in acute gout, whereas protein levels of T-bet were downregulated in PBMCs from acute gout patients and intercritical gout treated with MSU crystals in vitro as well. Transcription factor T-bet deficiency protects against MSU-induced gouty inflammation, suggesting that downregulation of T-bet could be a protective strategy and contribute to spontaneous remission of inflammation in acute gout.

Gout is a prevalent form of aseptic inflammation caused by the deposition of monosodium urate (MSU) crystals in joints or tissues. Triggering receptor expressed on myeloid cell-1 (TREM-1) is a superimmunoglobulin receptor expressed on innate immune cells including granulocytes, monocytes, and macrophages. TREM-1 serves as a link between innate immunity and adaptive immunity, playing a crucial role in regulating inflammation and immune response. The purpose of this study was to investigate the potential role of TREM-1 in THP-1 cells and peripheral blood mononuclear cells (PBMCs) from patients with gouty arthritis (GA). In the current study, we found that the mRNA and protein levels of TREM-1 increased in PBMCs from GA patients and soluble TREM-1 in plasma as well. In addition, an increased level of TREM-1 was observed in THP-1 treated with monosodium urate (MSU) in vitro, along with upregulation of proinflammatory cytokines. Moreover, upon specific inhibition of TREM-1, Toll-like receptor 4 (TLR-4), and myeloid differentiation factor 88 (MyD88), the levels of MyD88 and proinflammatory cytokines were decreased after MSU challenge in THP-1 cells. Interestingly, inhibition of TLR-4 could enhance the effect of TREM-1 inhibitor in MSU-induced inflammation. Taken together, our findings suggested that TREM-1 could accelerate MSU-induced acute inflammation. Inhibition of TREM-1 may provide a new strategy for alleviating acute gouty inflammation.

Resveratrol exerts an anti-inflammatory effect on collagen-induced arthritis and osteoarthritis in rats via activation of sirtuin 1 (SIRT1). Autophagy can be induced by resveratrol and leads to amelioration of interleukin-1 beta (IL-1β) release in vitro. We aimed to determine the anti-inflammatory mechanisms of resveratrol in patients with gout. Blood samples were obtained from patients with acute gout, intercritical gout (IG) and healthy controls (HC). The mRNA and protein levels of SIRT1 and nuclear factor-kappa B (NF-kB) p65 were determined in peripheral blood mononuclear cells (PBMCs) lysate from these patients. In the in vitro experiment, SIRT1, autophagy-related genes (beclin-1 and microtubule-associated protein 1 light-chain 3) and key genes involved in the gouty inflammatory pathway, including NF-κB p65, NLR family pyrin domain containing 3 (NLRP3), caspase-1 and IL-1β, were determined in PBMCs lysate or plasma from IG patients exposed to monosodium urate (MSU) crystals with or without resveratrol. The mRNA and protein levels of SIRT1 were downregulated in PBMCs from gout patients in comparison with HC. In the in vitro experiment, the protein levels of SIRT1 were downregulated in PBMCs from IG patients exposed to MSU crystals and were restored by resveratrol in a dose-dependent manner. Furthermore, high doses of resveratrol ameliorated the release of the inflammatory cytokine IL-1β. In addition, the mRNA levels of NLRP3 and NF-κB p65 were regulated by resveratrol, but caspase-1 and IL-1β were not. Furthermore, resveratrol promoted MSU-induced autophagy in PBMCs from patients with gout. These findings suggest that resveratrol ameliorates gouty inflammation via upregulation of SIRT1 to promote autophagy in patients with gout.

To analyze the levels of oxidized low density lipoprotein (ox-LDL) and inflammatory cytokines in the plasma of gout patients. The levels of ox-LDL, hypersensitive C-reactive protein (hs-CRP), interleukin-1β, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured in the plasma of 41 gout patients [28 in acute phase episode, 13 in intermittent phase (IP)], and in 40 healthy controls. The relationship between ox-LDL and inflammation was also explored by measuring the levels of several pro-inflammatory cytokines in the plasma. The plasma levels of ox-LDL, hs-CRP, IL-6 and TNF-α were significantly increased in patients with gout in the acute phase compared to those in the IP group and healthy controls (P

Gouty arthritis is the most common type of inflammatory and immune disease, and the prevalence and incidence of gout increases annually. Genetic variations in the DNA methyltransferases (DNMTs) gene have not, to the best of our knowledge, been reported to influence gene expression and to participate in the pathogenesis of gout. The aim of the present study was to investigate whether the DNMT1, DNMT3A and DNMT3B polymorphisms contribute to gout susceptibility. These polymorphisms were screened for in 336 gout patients and 306 healthy control subjects (from a South China population) for association with gout. The distribution frequencies of DNMT1 rs2228611 AA genotype (P=0.007) and A allele (P=0.002; odds ratio=1.508, 95% confidence interval=1.158-1.964) were found to be significantly increased in the gout patients when compared with those in the healthy control subjects. The rs1550117 in DNMT3A and rs2424913 in DNMT3B exhibited no significant associations with gout susceptibility between the patients and control subjects. These results demonstrated that the DNMT1 rs2228611 polymorphism may be involved in the pathogenesis of gout, while DNMT3A rs1550117 and DNMT3B rs2424913 did not show any obvious significance in the current study; thus, may not be used as risk factors to predict the susceptibility to gout. However, further studies are required to investigate the functions and regulatory mechanism of the polymorphisms of DNMTs in gout.

The morphological variation of Penaeus monodon was studied based on the morphometric analyses of samples collected throughout Banda Aceh, Khanom, Mozambique and Sanya. A total of 470 samples were investigated using eight measurements. Multivariate analyses [principal components (PCA), discriminant function (DFA) and cluster analyses (CA)] revealed obvious morphometric differences among the four geographical populations. PCA indicated that the first three components of the females and the first two components of the males accounted for 75.17% and 71.84% of the total morphological variability respectively. In DFA, the overall assignment of female and male individuals into their original population was 78.95% and 84.37% respectively. For females, the proportion of individuals correctly classified into their original population was 76.0%, 92.8%, 92.6% and 54.5% for population 1, 2, 3 and 4 respectively. For males, the proportion was 97.2%, 68.1%, 100% and 72.2% respectively. For females and males, CA showed that the four populations could be divided into two main clusters of morphological characteristics. CA also indicated that the morphological variation of population 3 was greater, whereas the morphology of population 2 was strikingly similar to that of population 4.

Gout patients have a high incidence of atherosclerotic coronary heart disease. Low serum paraoxonase (PON) activity is considered a risk factor for atherosclerosis. The relationships among paraoxonase-1 (PON1) activity, oxidative stress parameters, and atherosclerosis in gout is not known. Therefore, we determined the plasma levels of malondialdehyde (MDA), oxidized low-density lipoprotein (Ox-LDL), and activities of PON1/superoxide dismutase (SOD) activities in 49 gout patients (mean age 44.2 ± 7.0 years) and 42 healthy, age-matched controls (mean age 45.0 ± 9.3 years). PON1 was measured spectrophotometrically, MDA by thiobarbituric acid method, SOD by Griess reaction, and Ox-LDL by sandwich ELISA. Lipid and other biochemical parameters were determined by routine laboratory methods. In gout patients, PON1/SOD activities and MDA/Ox-LDL levels were 131.3 ± 25.3/75.3 ± 28.9 kU l(-1) and 6.12 ± 1.67 nmol ml(-1)/690.1 ± 180.2 μg l(-1), respectively. In controls, these were 172.5 ± 27.8/94.0 ± 26.3 kU l(-1) and 4.10 ± 1.25 nmol ml(-1)/452.3 ± 152.1 μg l(-1), respectively. Thus, in gout patients, there was a significant decrease in PON1 (P < 0.01) and SOD (P < 0.05) activities, and an increase in MDA (P < 0.01) and Ox-LDL (P < 0.01) levels compared with controls. PON1 activity correlated positively with SOD (P < 0.05), and negatively with MDA (P < 0.01) and Ox-LDL (P < 0.01). These results suggest that gout patients were in a state of oxidative stress and the protective effects of HDL against atherosclerosis maybe dependent on PON1 activity. These findings may explain in part the reported increase in cardiovascular mortality in gout patients.

Background The findings of a previous study by Jin et al. have shown that microRNA (miR)-155 was upregulated in patients with acute gouty arthritis and enhanced the proinflammatory cytokines. There is no direct evidence to support that miR-155 is indeed involved in monosodium urate (MSU)-induced inflammatory responses in vivo. The aim of this study was to investigate the role of miR-155 knock-out (KO) or knock-in (KI) mice in MSU-induced animal models to mimic acute gout. Methods MiR-155 expression in cultured bone marrow-derived macrophages (BMDMs) from miR-155 KO, miR-155 KI, and wild-type (WT) mice treated with MSU crystals in vitro was detected by real-time quantitative polymerase chain reaction (qPCR). MiR-155 KO and WT mice were used to induce an acute gouty inflammatory response with MSU crystals including models of foot pad inflammation, ankle arthritis, air pouch inflammation, and peritonitis. Furthermore, the proinflammatory interleukin (IL)-1β levels in lavage fluids from air pouch and peritoneal cavity models were measured by enzyme-linked immunosorbent assay (ELISA), and tumor necrosis factor (TNF)-α production from BMDMs of miR-155 KI mice treated with MSU were measured by flow cytometry. Results MiR-155 expression was quickly upregulated in BMDMs from WT mice following MSU treatment in vitro. In comparison with WT mice in vivo, the swelling index of miR-155 KO mice showed no significant difference in the murine foot pad and ankle arthritis models for the indicated different time points. There were similar changes in total cell numbers of lavage fluids in the air pouch and peritoneal cavity models between miR-155 KO and WT mice following MSU crystal injection. Moreover, the IL-1β levels of lavage fluids in the air pouch and peritonitis models from miR-155 KO mice were almost the same as those from WT mice. TNF-α levels were comparable from BMDMs treated with MSU crystals in vitro between miR-155 KI mice and WT mice. Conclusions MiR-155 is dispensable in MSU-induced gouty inflammation in mice. Deletion of miR-155 might not be an effective therapeutic approach to relieve the inflammation in acute gout.

This is a cross-sectional study to assess the prevalence and causes of anemia in the primary Sjögren's syndrome (pSS). One hundred and thirty-two consecutive patients with pSS were enrolled into the study. Standard hematological and immunological tests and examination of bone marrow were performed. Anemia occurred in 45 (34.1%) patients. The causes of anemia included anemia of chronic disease (69%), autoimmune hemolytic anemia (AIHA, 18%), iron deficiency anemia (9%) and other causes (4%), of which AIHA caused the most severe anemia. The prevalence of ANA, anti-Ro/SSA, and anti-La/SSB was much higher in patients with anemia than those without anemia. Anticardiolipin antibodies were most commonly detected in AIHA; the prevalence of IgG and hypocomplementemia in AIHA was much higher in patients without anemia. Abnormal bone marrow changes were observed in two cases with anemia, one with morphological changes in the myeloid, megakaryocytic, and erythroid lineages and one with hypocellularity in the erythroid lineage. Therefore, pSS patients with anemia may be associated with destruction of peripheral mature blood cells, impaired red cells production, and hematopoietic abnormalities due to an immune mechanism, although the concrete pathogenesis is still unclear.

The simulation of the high order Laue zone (HOLZ) diffractions of monoclinic and triclinic crystals is a very complicated problem. The conventional multislice (MS) method suffers from the problem of infinity of the phase grating size. To avoid the difficulty of the infinity, Chen et al. arranged the phase grating plane along the ab plane of the crystal lattice. In this paper we introduce a new method which allows the incident and exit wavefunction planes perpendicular to the zone axis without the difficulty of infinity. We name the method half analytical method. The results calculated by half analytical method are in good agreement with those calculated by the conventional MS method.

We undertook this study to determine whether the altered expression of telomeric proteins TPP1 and POT1 in fibroblast-like synovial cells (FLS) could provide insights into the pathogenesis of rheumatoid arthritis (RA). FLS were isolated from patients with RA, osteoarthritis (OA) and traumatic joint disease, and cultured in vitro. TPP1 and POT1 mRNA level of FLS were measured using real-time quantitative polymerase chain reaction (RT-qPCR) in 42 RA, 23 OA and 13 healthy cases. Immunofluorescence staining and Western blot were used to detect the expression of TPP1 and POT1 protein. Expression of TPP1 and POT1 mRNA was significantly reduced in RA cases (P0.001, respectively), and no significant difference was observed between OA and healthy cases (P0.05, respectively). Confocal microscopy images showed TPP1 and POT1 proteins mainly located in nucleus of FLS. Western blot demonstrated that TPP1 protein level was significantly reduced in RA cases (P0.001), and POT1 protein expression was not statistical significance among RA, OA patients and healthy cases (P0.05). Significant negative correlation was observed between level of TPP1 mRNA and titers of anti-CCP antibody (P0.001), RF (P0.01). Altered expression of TPP1 might contribute to persistent proliferation of FLS in RA, further study on functions of telomeric proteins in RA would be needed.

Er(3+)-Doped Germanium Bismuthate Glass was fabricated and characterized. The absorption spectrum and up-conversion spectrum of glass were studied. The Judd-Oflet intensity parameters omega(t) (t = 2, 4, 6), determined based on Judd-Ofelt theory, were found to be omega2 = 3.35 x 10(-20) cm2, omega4 = 1.34 x 10(-20) cm2, omega6 = 0.67 x 10(-20) cm2. Frequency up-conversion of Er(3+)-doped germanium bismuthate glass has been investigated. The up-conversion mechanisms are discussed under 808 nm and 980 nm excitation. Stimulated emission cross-section of 4I(13/2) --4I(15/2) transition was calculated by McCumber theory. Compared to other host glasses, the emission property of Er(3+)-doped germanium bismuthate glasses has advantage over those of silicate, phosphate and germinate glasses. Er(3+)-doped germanium bismuth glasses are promising upconversion optical and optic-communication materials.

The simulation of exit wavefunctions of a TEM sample is carried out by both the conventional multislice (C-MS) method and the real space multislice (RS-MS) method, with a series of different slice thicknesses. Surprisingly, the results calculated by the RS-MS method remain constant to seven significant figures when the slice thicknesses are changed within a wide range, while those calculated by the C-MS method change significantly. From the mathematical point of view, the C-MS method is only a first order approximation of the RS-MS method. Thus, the calculation precision of the RS-MS method is much higher than that of the C-MS method. Or to achieve the same precision, the slice thickness for the RS-MS method can be taken as two orders of magnitude larger than for the C-MS method in the simulation. As a result, the calculation speed for the RS-MS method may be even faster than that for the C-MS method in some cases. For the two advantages stated above, the RS-MS method may be more suitable for precise calculations.