Combined effects of cadmium and copper on the expression of antioxidant enzyme — coding genes in the polychaete, Perinereis nuntia

Polychaetes have been used as useful model organisms for environmental pollution monitoring in aquatic sediments. Here, we investigated the combined effect of copper (50, 100 and 200 μg/L) and cadmium (50 μg/L) on the expression of antioxidant enzymecoding genes (seven GST isoforms, Mn-SOD and Cu/Zn-SOD) in the marine polychaete Perinereis nuntia by quantitative real-time RT-PCR. As a result, SOD genes, especially Cu/Zn-SOD significantly increased up to 48 h after exposure to a mixture of Cu and Cd in a time and concentration-dependent manner more than in 50 μg/L Cd alone exposure. Similar expression patterns were observed in most GST isoforms. In particular, GST-omega and GST-sigma gene expression were highly upregulated in response to a combined stress of Cd and Cu. These findings suggest that such genes would be useful as a potential molecular biomarker for monitoring of combined environmental pollutions in aquatic ecosystem.     

Double saccadic pulses and macrosaccadic oscillations from a focal brainstem lesion

Double saccadic pulses (DSP) are saccadic intrusions that consist of an initial saccade away from a fixation followed immediately by a return saccade back to the fixation. DSP have been reported in patients with presumed multiple sclerosis and metabolic encephalopathy. However, DSP have not been described in a circumscribed brain lesion. We report a man who developed almost continuous DSP with intervening macrosaccadic oscillations from a circumscribed lesion in the dorsal pontine tegmentum which extended up to the midbrain level and spared the nucleus raphe interpositus where the pause cells reside. Damage to the projections from the superior colliculus to omnipause neurons and resultant dysfunction of omnipause neuron may be a mechanism of saccadic intrusions and oscillations observed in our patient with a circumscribed brainstem lesion.     

Suppressive effect of non-anaphylactogenic anti-IgE antibody on the development of dextran sulfate sodium-induced colitis

Inflammatory bowel disease (IBD) is a spectrum of immune-mediated chronic disorders of the intestine. Patients with IBD tend to exhibit significantly elevated levels of IgE in their serum. In general, the pathogenesis of IBD exhibits inflammatory events such as immunoglobulin E (IgE)-mediated hypersensitivity. We examined the effect of the non-anaphylactogenic anti-IgE antibody, which has been known to block IgE functions, in an animal model of ulcerative colitis induced by the oral intake of dextran sulfate sodium (DSS) for seven days. The non-anaphylactogenic anti-IgE antibody was subcutaneously injected on day 0 of DSS treatment. The disease activity index (DAI) was calculated by scoring intestinal states, including body weight loss, diarrhea, and rectal bleeding, and the activities of myeloperoxidase (MPO) and chymase were measured in the colon tissue. In addition, the expression of tumor necrosis factor (TNF)-alpha and cyclooxygenase (COX)-2 was determined by Western blotting. Administration of the anti-IgE antibody markedly reduced the histological damage to the colon and the DAI increment exhibited by the DSS-induced colitis. The anti-IgE antibody also significantly suppressed the activities of MPO and chymase as well as the expression of TNF-alpha and COX-2 in the DSS-treated colon tissue. Furthermore, the elevation of IgE levels in serum was induced by DSS and reduced by anti-IgE antibody injection. Thus, these results indicate that the IgE response played an important role in the clinical signs and the expression of inflammatory mediators in a colitis model caused by DSS treatment, suggesting that the non-anaphylactogenic anti-IgE antibody may be a useful therapeutic agent for ulcerative colitis.     

Z39Ig is expressed on macrophages and may mediate inflammatory reactions in arthritis and atherosclerosis

Z39Ig is a transmembrane protein containing two Ig homology domains with unknown functions. Immunohistochemical analyses of human carotid atherosclerotic plaques detected Z39Ig staining in areas rich in foamy macrophages. Z39Ig staining was also observed in macrophages in the lining layers and sublining areas of rheumatoid arthritis synovium. Z39Ig staining in the osteoarthritis synovium was restricted to macrophages in the lining layers. To identify the role(s) of Z39Ig in the function of macrophages, we used human monocytic cell lines TF-1A (Z39Ig-negative) and THP-1 (Z39Ig-positive). The expression of Z39Ig was induced in TF-1A cells ,when they were differentiated into macrophages by treatment with PMA. The stimulation of PMA-treated TF-1A or THP-1 cells with immobilized anti-Z39Ig mAb induced the secretion of IL-8 and matrix metalloproteinase (MMP)-9, which was dependent on NF-kappaB activation. These data indicate that the macrophage Z39Ig is involved in the pathogenesis of inflammatory diseases through chemokine induction, which will promote the migration of inflammatory cells into the lesion area, and MMP-9 induction, which will contribute to cartilage destruction or extracellular matrix degradation.     

Translation and validation of the Korean version of the Sarcopenia Quality of Life (SarQoL-K®) questionnaire and applicability with the SARC-F screening tool

Quality of Life Research - The purpose of this paper was to translate and validate into the Korea language and setting the Sarcopenia Quality of Life (SarQoL®) questionnaire. The participants...     

Efficacy and Safety of Clinically Driven Low-Dose Treatment with Direct Oral Anticoagulants in Asians with Atrial Fibrillation: a Systematic Review and Meta-analysis

Cardiovascular Drugs and Therapy - Although clinically driven low-dose (CDLD) treatment with direct oral anticoagulants (DOACs) is frequently administered to Asian patients with atrial...     

Quercetin, a bioflavonoid, accelerates TNF-alpha-induced growth inhibition and apoptosis in MC3T3-E1 osteoblastic cells

The bioflavonoid quercetin is believed to play an important role in preventing bone loss by affecting osteoclastogenesis and regulating many systemic and local factors including hormones and cytokines. This study examined how quercetin acts on tumor necrosis factor-alpha (TNF-alpha)-mediated growth inhibition and apoptosis in MC3T3-E1 osteoblastic cells. Tritium uptake assay showed that a quercetin treatment accelerated TNF-alpha-induced inhibition of DNA synthesis in the cells in a dose-dependent manner. Both the 3-(4,5-dimethylthiazol-2yl-)-2,5-diphenyl tetrazolium bromide and trypan blue staining assays also showed the quercetin-mediated facilitation of TNF-alpha-induced cytotoxicity in the cells. Apoptosis assays revealed an accelerating effect of quercetin on TNF-alpha-induced apoptosis in MC3T3-E1 cells. In addition, Fas activation and poly (ADP ribose) polymerase cleavage are thought to be closely associated with the TNF-alpha-induced apoptosis and its acceleration by the quercetin treatment in the cells. Collectively, this study showed that quercetin accelerates the TNF-alpha-induced growth inhibition and apoptosis in MC3T3-E1 osteoblastic cells.