Pseudo-Journals and Pseudo-Conferences: the Characteristics and Preventive Measures

This article explains the relationship between open-access publications and pseudo-journals, and explores their characteristics including predatory journals and journal hijackers. Pseudo-journals and pseudo-conferences cause the disruption of academic development by spreading low quality information as well as the violation of research ethics by abusing research funds. Finally, preventive measures are described from the perspective of journal authors/researchers, institutions/funding organizations, and journal editors.

Do Helper T Cell Subtypes in Lymphocytic Thyroiditis Play a Role in the Antitumor Effect?

BACKGROUND: Papillary thyroid carcinoma (PTC) is frequently accompanied by lymphocytic thyroiditis (LT). Some reports claim that Hashimoto's thyroiditis (the clinical form of LT) enhances the likelihood of PTC; however, others suggest that LT has antitumor activity. This study was aimed to find out the relationship between the patterns of helper T cell (Th) cytokines in thyroid tissue of PTC with or without LT and the clinicopathological manifestation of PTC. METHODS: Fresh surgical samples of PTC with (13 cases) or without (10 cases) LT were used. The prognostic parameters (tumor size, extra-thyroidal extension of PTC, and lymph node metastasis) were analyzed. The mRNA levels of two subtypes of Th cytokines, Th1 (tumor necrosis factor α [TNF-α], interferon γ [IFN-γ ], and interleukin [IL] 2) and Th2 (IL-4 and IL-10), were analyzed. Because most PTC cases were microcarcinomas and recent cases without clinical follow-up, negative or faint p27 immunoreactivity was used as a surrogate marker for lymph node metastasis. RESULTS: PTC with LT cases showed significantly higher expression of TNF-α (p = .043), IFN-γ (p < .010), IL-4 (p = .015) than those without LT cases. Although the data were not statistically significant, all analyzed cytokines (except for IL-4) were highly expressed in the cases with higher expression of p27 surrogate marker. CONCLUSIONS: These results indicate that mixed Th1 (TNF-α, IFN-γ , and IL-2) and Th2 (IL-10) immunity might play a role in the antitumor effect in terms of lymph node metastasis.

Acute exposure to silica nanoparticles aggravate airway inflammation: different effects according to surface characteristics

Silica nanoparticles (SNPs) are widely used in many scientific and industrial fields despite the lack of proper evaluation of their potential toxicity. This study examined the effects of acute exposure to SNPs, either alone or in conjunction with ovalbumin (OVA), by studying the respiratory systems in exposed mouse models. Three types of SNPs were used: spherical SNPs (S-SNPs), mesoporous SNPs (M-SNPs), and PEGylated SNPs (P-SNPs). In the acute SNP exposure model performed, 6-week-old BALB/c female mice were intranasally inoculated with SNPs for 3 consecutive days. In the OVA/SNPs asthma model, the mice were sensitized two times via the peritoneal route with OVA. Additionally, the mice endured OVA with or without SNP challenges intranasally. Acute SNP exposure induced significant airway inflammation and airway hyper-responsiveness, particularly in the S-SNP group. In OVA/SNPs asthma models, OVA with SNP-treated group showed significant airway inflammation, more than those treated with only OVA and without SNPs. In these models, the P-SNP group induced lower levels of inflammation on airways than both the S-SNP or M-SNP groups. Interleukin (IL)-5, IL-13, IL-1beta and interferon-gamma levels correlated with airway inflammation in the tested models, without statistical significance. In the mouse models studied, increased airway inflammation was associated with acute SNPs exposure, whether exposed solely to SNPs or SNPs in conjunction with OVA. P-SNPs appear to be relatively safer for clinical use than S-SNPs and M-SNPs, as determined by lower observed toxicity and airway system inflammation.

Contrasting Roles of Different Endoglin Forms in Atherosclerosis

Endoglin (also known as CD105 or TGF-beta type III receptor) is a co-receptor involved in TGF-beta signaling. In atherosclerosis, TGF-beta signaling is crucial in regulating disease progression owing to its anti-inflammatory effects as well as its inhibitory effects on smooth muscle cell proliferation and migration. Endoglin is a regulator of TGF-beta signaling, but its role in atherosclerosis has yet to be defined. This review focuses on the roles of the various forms of endoglin in atherosclerosis. The expression of the two isoforms of endoglin (long-form and short-form) is increased in atherosclerotic lesions, and the expression of the soluble forms of endoglin is upregulated in sera of patients with hypercholesterolemia and atherosclerosis. Interestingly, long-form endoglin shows an atheroprotective effect via the induction of eNOS expression, while short-form and soluble endoglin enhance atherogenesis by inhibiting eNOS expression and TGF-beta signaling. This review summarizes evidence suggesting that the different forms of endoglin have distinct roles in atherosclerosis.

Immunostimulatory Effects of Silica Nanoparticles in Human Monocytes

Amorphous silica particles, whose applications are increasing in many biomedical fields, are known to be less toxic than crystalline silica. In this study, the inflammatory effects of amorphous silica nanoparticles were investigated using 30-nm amorphous silica nanoparticles and human peripheral blood mononuclear cells (PBMCs) or purified monocytes. As a result, production of IL-1beta and IL-8 were increased. In addition, the mitochondrial reactive oxygen species (ROS) was detected, which may lead to mitochondrial membrane disruption. Most importantly, inflammasome formation was observed. Therefore, these results provide immunological information about amorphous silica nanoparticles and suggest that amorphous silica nanoparticles can evoke innate immune reactions in human monocytes through production of IL-1beta and IL-8.

The Effects of Silica Nanoparticles in Macrophage Cells

Silica nanoparticles, which are applicable in many industrial fields, have been reported to induce cellular changes such as cytotoxicity in various cells and fibrosis in lungs. Because the immune system is the primary targeting organ reacting to internalized exogenous nanoparticles, we tried to figure out the immunostimulatory effect of silica nanoparticles in macrophages using differently sized silica nanoparticles. Using U937 cells we assessed cytotoxicity by CCK-8 assay, ROS generation by CM-H2DCFDA, intracellular Ca++ levels by staining with Fluo4-AM and IL-8 production by ELISA. At non-toxic concentration, the intracellular Ca++ level has increased immediately after exposure to 15 nm particles, not to larger particles. ROS generation was detected significantly in response to 15 nm particles. However, all three different sizes of silica nanoparticles induced IL-8 production. 15 nm silica nanoparticles are more stimulatory than larger particles in cytotoxicity, intracellular Ca++ increase and ROS generation. But IL-8 production was induced to same levels with 50 or 100 nm particles. Therefore, IL-8 production induced by silica nanoparticles may be dependent on other mechanisms rather than intracellular Ca++ increase and ROS generation.

Silver Nanoparticles as a Smart Antimicrobial Agent

In modern medicine the resistance to conventional antibiotics is becoming a serious concern due to high instances of mortality. Several metallic nanoparticles are suggested as promising anti-microbial agents against multidrug-resistant bacteria and some viruses. Among the nanoparticles mentioned, we review the recent finding which demonstrate the impact of silver nanoparticles on antimicrobial activities and recommend them as a potential candidate for restraining infections.

Phagocytosis and Endocytosis of Silver Nanoparticles Induce Interleukin-8 Production in Human Macrophages

Phagocytosis or endocytosis by macrophages is critical to the uptake of fine particles, including nanoparticles, in order to initiate toxic effects in cells. Here, our data enhance the understanding of the process of internalization of silver nanoparticles by macrophages. When macrophages were pre-treated with inhibitors to phagocytosis, caveolin-mediated endocytosis, or clathrin-mediated endocytosis, prior to exposure to silver nanoparticles, Interleukin-8 (IL-8) production was inhibited. Although cell death was not reduced, the inflammatory response by macrophages was compromised by phagocytosis and endocytosis inhibitors.

CKD-712, (S)-1-(alpha-naphthylmethyl)-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Inhibits the NF-kappaB Activation and Augments Akt Activation during TLR4 Signaling

Since CKD-712 has been developed as an anti-inflammatory agent, we examined the effect of CKD-712 during TLR4 signaling. Using HEK293 cells expressing TLR4, CKD-712 was pre-treated 1 hr before LPS stimulation. Activation of NF-kappaB was assessed by promoter assay. The activation of ERK, JNK, p38, IRF3 and Akt was measured by western blotting. CKD-712 inhibited the NF-kappaB signaling triggered by LPS. The activation of ERK, JNK, p38 or IRF3 was not inhibited by CKD-712. On the contrary the activation of these molecules was augmented slightly. The activation of Akt with stimulation of LPS was also enhanced with CKD-712 pre-treatment at lower concentration, but was inhibited at higher concentration. We suggest that during TLR4 signaling CKD-712 inhibits NF-kappaB activation. However, CKD-712 augmented the activation of Akt as well as Map kinases. Therefore, we suggest that CKD-712 might have a role as an immunomodulator.

Ribosomal Protein L19 and L22 Modulate TLR3 Signaling

BACKGROUND: Toll-like receptor 3 (TLR3) recognizes double-stranded RNA (dsRNA) and induces inflammation. In this study we attempted to ascertain if there are endogenous host molecules controlling the production of cytokines and chemokines. Two candidates, ribosomal protein L19 and L22, were analyzed to determine if they influence cytokine production followed by TLR3 activation. In this study we report that L19 acts upon production of IP-10 or IL-8 differently in glioblastoma cells. METHODS: L19 or L22 was transfected into HEK293-TLR3, A549 or A172 cells. After treatment with several inhibitors of NF-kB, PI3K, p38 or ERK, production of IL-8 or IP-10 was measured by ELISA. siRNA was introduced to suppress expression of L19. After Vesicular stomatitis virus infection, viral multiplication was measured by western blot. RESULTS: L19 increased ERK activation to produce IL-8. In A172 cells, in which TLR3 is expressed at endosomes, L19 inhibited interferon regulatory factor 3 (IRF3) activation and IP-10 production to facilitate viral multiplication, whereas L19 inhibited viral multiplication in A549 cells bearing TLR3 on their cell membrane. CONCLUSION: Our results suggest that L19 regulates TLR3 signaling, which is cell type specific and may be involved in pathogenesis of autoimmune diseases and chronic inflammatory diseases.

The Impact of Nanomaterials in Immune System

As a nanotechnology has been actively applied to the overall areas of scientific fields, it is necessary to understand the characteristic features, physical behaviors and the potential effects of exposure to nanomaterials and their toxicity. In this article we review the immunological influences induced by several nanomaterials and emphasize establishment of the animal models to estimate the impact of these nanomaterials on development of immunological diseases.

An Introduction to the New Web Site of the Journal of the Korean Medical Association

The Journal of the Korean Medical Association (JKMA) established a new web site in July, 2010 available at http://jkma.org/. Here, we introduce the basic structure and concept of the new web site. The new web site provides current medical information from Korea to KMA members as well as global readers. The history of Korean medicine will also be organized in an easily accessible. Starting from this basic platform, JKMA will improve and expand other online functions in the near future. We hope every member of the Korean Medical Association enjoys browsing the content of JKMA through the new site and using the information they find in their clinical practice.

Retraction: Bilateral Popliteal Artery Aneurysms with Rupture and Pseudoaneurysm Formation on the Left

This article has been found to be a duplicate publication.

Production of TNF-alpha and IL-6 in Macrophages by Mycobacterial Protein Antigens

BACKGROUND: Mycobacterial antigens released as PIM, LM, LAM, lipoproteins and other cellular factors may contribute to macrophage and dendritic cell activation through pattern recognition receptors such as TLRs. In this study, we assessed cytokine production and ERK activation with stimulation of several major mycobacterial antigens. METHODS: Purified mycobacterial antigens (10, 22, 30, 38kappaDa) and recombinant antigens (6, 16, 19, 38kappaDa, Ag85A antigen) were studied. The production of cytokines (TNF-alpha, IL-12, IL-6) was measured by ELISA. The ERK activation was detected by western blotting. The expression of TLR2 or TLR4 was measured by flow cytometry. RESULTS: Among purified antigens only 30kappaDa antigen induced production of IL-6 or TNF-alpha in THP-1 macrophage cells. When THP-1 macrophage cells were treated with 30kappaDa antigen, phosphorylation of ERK was detected. ERK activation also occurred in TLR2 transfectant HEK293 cells with 30kappaDa antigen stimulation. CONCLUSION: 30kappaDa antigen is one of the major mycobacterial antigens inducing cytokine production and MAP kinases phosphorylation in macrophages.

Hydrogen Peroxide Upregulates TNF-Related Apoptosis-Inducing Ligand (TRAIL) Expression in Human Astroglial Cells, and Augments Apoptosis of T Cells

The brain is particularly vulnerable to oxygen free radicals, and these radicals have been implicated in the pathology of several neurological disorders. In this study, the modulation of TNF-related apoptosis-inducing ligand (TRAIL) expression by oxidative stress was shown in LN215 cells, an astroglioma cell line. Hydrogen peroxide (H2O2) treatment increased TRAIL expression in LN215 cells and H2O2-induced TRAIL augmented apoptosis in Peer cells, a cell line sensitive to TRAIL- mediated cell death. Our findings suggest that the upregulation of TRAIL in astroglial cells may abrogate immune cell effector functions.

Human Brain Astrocytes Mediate TRAIL-mediated Apoptosis after Treatment with IFN-gamma

TNF-related apoptosis inducing ligand (TRAIL) expressions were studied in primary human brain astrocytes in response to pro-inflammatory cytokines. When astrocytes were treated with IL-1beta TNF-alphaor IFN-gamma TRAIL was induced in cultured fetal astrocytes. In particular, IFN-gammainduced the highest levels of TRAIL in cultured astrocytes. When astrocytes were pre-reated with IFN-gamma they induced apoptosis in TRAIL-sensitive Peer cells. Our results suggest that IFN-gamma modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain.

Human Brain Astrocytes Mediate TRAIL-mediated Apoptosis after Treatment with IFN-gamma

TNF-related apoptosis inducing ligand (TRAIL) expressions were studied in primary human brain astrocytes in response to pro-inflammatory cytokines. When astrocytes were treated with IL-1beta TNF-alphaor IFN-gamma TRAIL was induced in cultured fetal astrocytes. In particular, IFN-gammainduced the highest levels of TRAIL in cultured astrocytes. When astrocytes were pre-reated with IFN-gamma they induced apoptosis in TRAIL-sensitive Peer cells. Our results suggest that IFN-gamma modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain.

Peptide Mimotopes of Neisseria meningitidis Group B Capsular Polysaccharide

The antigenic similarity between Neisseria meningitidis group B (NMGB) capsular polysaccharide (PS) and human polysialic acid (PSA) has hampered the development of a NMGB PS-based vaccine. But the possibility of a safe vaccine based on NMGB PS has been demonstrated by the existence of the NMGB PS-associated nonautoreactive epitope, which is distinct from those present on human PSA. To obtain peptide mimotopes of NMGB PS, we used HmenB3, a protective and nonautoreactive monoclonal antibody, to screen a phage library with 12 amino acids. We obtained 23 phage clones that bound to HmenB3 but not in the presence of E. coli K1 PS [which is alpha (2-8) -linked PSA like NMGB PS]. The clones contained 3 mimotopes and differed from previously described NMGB PS mimotopes. Immunization with a synthetic peptide of one mimotope elicited anti-NMGB antibodies in BALB/c mice. These mimotopes may be useful in the development of group B meningococcal vaccines.

IFN-gamma Regulates Expression of BRG1 Associated Factor 155/170 and Sensitivity to Steroid in Astrocytes

BACKGROUND: The expression of BRG1 associated factors (BAF) 155 and BAF 170 in response to IFN-gamma or TNF-alpha was studied in astrocytoma cell lines and primary astrocytes. BAFs are complexed with BRG1 and are also associated with activated glucocorticoid for glucocorticoid trans-activation. METHODS: IFN-gamma was pretreated for 18 hrs and cells were incubated with IL-1 or TNF-alpha for 72 hrs or 96 hrs with different concentrations of steroid. Cell death was measured by LDH assay. BAF expression was assayed by RT-PCR. RESULTS: IFN-gamma increased cell death by dexamethasone in LN215 cells but not in LN319 cells. The IFN-gamma increased the expression of BAF 155 and BAF 170 in adult astrocytes and LN215 cells, but IFN-gamma decreased the expression of BAF 155/170 in LN319 cells. The effect of IFN-gamma on the expression of BAF was not as clear in fetal astrocytes as it was in adult astrocytes. CONCLUSION: Our results suggest cytokines produced during immune reaction or immunotherapy may modulate steroid susceptibility of astrocytes and astrocytoma cells by influencing the expression of BAFs.

Cloning of TLR3 Isoform

Toll-like receptor (TLR) 3 is a member of the TLR family that confers innate immunity by recognizing viral pathogens. Herein, we report that the TLR3 isoform is expressed on human primary cells and cell lines. This isoform has 2, 520 bp cDNAs compared to the 2, 712 bp of full cDNA, is produced by deletion of an intron-like sequence within exon 4 and is co-expressed with wild type TLR3 in primary human astrocytes and glioblastoma cell lines. This finding suggests the TLR3 isoform in astrocytes may have a different immunological role for binding ligands during the immune response in brain.