Scutellaria baicalensis

Antimycin A (AMA) damages mitochondria by inhibiting mitochondrial electron transport and can produce reactive oxygen species (ROS). ROS formation, aging, and reduction of mitochondrial biogenesis contribute to mitochondrial dysfunction. The present study sought to investigate extracts of Scutellaria baicalensis and its flavonoids (baicalin, baicalein, and wogonin), whether they could protect mitochondria against oxidative damage. The viability of L6 cells treated with AMA increased in the presence of flavonoids and extracts of S. baicalensis. ATP production decreased in the AMA treated group, but increased by 50% in cells treated with flavonoids (except wogonin) and extracts of S. baicalensis compared to AMA-treated group. AMA treatment caused a significant reduction (depolarized) in mitochondrial membrane potential (MMP), whereas flavonoid treatment induced a significant increase in MMP. Mitochondrial superoxide levels increased in AMA treated cells, whereas its levels decreased when cells were treated with flavonoids or extracts of S. baicalensis. L6 cells treated with flavonoids and extracts of S. baicalensis increased their levels of protein expression compared with AMA-treated cells, especially water extracts performed the highest levels of protein expression. These results suggest that the S. baicalensis extracts and flavonoids protect against AMA-induced mitochondrial dysfunction by increasing ATP production, upregulating MMP, and enhancing mitochondrial function

A Case of Wernicke's Encephalopathy Following Fluorouracil-based Chemotherapy

The pyrimidine antimetabolite 5-fluorouracil (5-FU) is a chemotherapeutic agent used widely for various tumors. Common side effects of 5-FU are related to its effects on the bone marrow and gastrointestinal epithelium. Neurotoxicity caused by 5-FU is uncommon, although acute and delayed forms have been reported. Wernicke's encephalopathy is an acute, neuropsychiatric syndrome resulting from thiamine deficiency, and has significant morbidity and mortality. Central nervous system neurotoxicity such as Wernicke's encephalopathy following chemotherapy with 5-FU has been reported rarely, although it has been suggested that 5-FU can produce adverse neurological effects by causing thiamine deficiency. We report a patient with Wernicke's encephalopathy, reversible with thiamine therapy, associated with 5-FU-based chemotherapy

Economic Development of North Korea: International Trade Based Development Policy and Legal Reform

This article provides a rare account of the law and development policies of North Korea. Much of North Korea has not been known to the outside world except its nuclear ambitions and political clashes with the United States and its allies. Little known to the outside world, North Korea achieved rapid economic development in the 1950s through early 60s, through effective mobilization of resources. However, since the 70s, North Korea experienced economic downturns that eventually led to its economic crisis in the 90s. This chapter provides a discussion of North Korea's early economic success and the subsequent problems that it experienced. The article also provides an analysis of possible economic reforms, public health and development issues, and the role of international trade in economic development in North Korea.

妊娠マウスを用いた先天性トキソプラズマ症モデルにおけるRT-PCRによるサイトカイン産生の解析

To explore the mechanisms of immune responses of host to Toxoplasma gondii ( T. gondii) infection in pregnant mice, we evaluated roles of cytokines [interferon gamma (IFN-y), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and interleukin 4 (IL-4)] J by measuring mRNAS of these cytokines in placentas, lungs and spleens. The pathogenic effects of time and duration of the Fukaya infection on cytokine mRNA levels in pregnant mice were analyzed. The abundance of mRNAS encoding these cytokines was measured by reverse transcriptase (RT)-PCR at early and late stages of pregnancy in various organs of both susceptible C57BL/6 and resistant BALB/c pregnant mice infected with T. gondii. IFN-y and TNF-α but not IL-6 or IL-4, were predominant in the immune responses of placentas, lungs and spleens of BALB/ c and C57BL/6 mice during T. gondii infection. Levels of IFN-y and TNF-α mRNA in placentas of early stage pregnant BALB/c mice (infected at one-week pregnancy and examined on day 4 after infection; 1W4D) were higher than those in corresponding C57BL/6 pregnant mice, which might correlate with the fact that higher parasite numbers in placentas and lungs of C57BL/6 mice (infected at one-week pregnancy and examined on day 11 after the Fukaya infection; 1W11D) were observed than those in placentas and lungs of corresponding BALB/c mice, but not correlate with the result of parasite numbers (T. gondii No./mg tissue) in spleens of C57BL/6 (O) and BALB/c (120±56) pregnant mice. In the late stage of pregnancy, levels of IFN-y and TNF-α did not show definite correlations with T. gondii loads in placentas, lungs and spleens. These results indicate that endogenous IFN-y and TNF-α of early stage pregnancy may be essential for inhibition of T. gondii growth in some organs (placentas and lungs), but not in spleens, and the mechanisms of genetic influence involved in the susceptibility and resistance to acute T. gondii infection may include several immune responses acting together

Toll-Like Receptor 4 Mediates Tolerance in Macrophages Stimulated with Toxoplasma gondii-Derived Heat Shock Protein 70

Peritoneal macrophages (PMs) from toll-like receptor 4 (TLR4)-deficient and wild-type (WT) mice were responsive to recombinant Toxoplasma gondii-derived heat shock protein 70 (rTgHSP70) and natural TgHSP70 (nTgHSP70) in NO release, but those from TLR2-, myeloid differentiation factor 88 (MyD88)-, and interleukin-1R-associated kinase 4 (IRAK4)-deficient mice were not. Polymyxin B did not inhibit PM activation by TgHSP70 and nTgHSP70 from WT and TLR4-deficient mice, while it inhibited PM activation by lipopolysaccharide. Pretreatment of PMs from WT but not from TLR4-deficient mice with rTgHSP70 resulted in suppression of NO release on restimulation with rTgHSP70. Similarly, pretreatment of PMs from WT but not TLR4-deficient mice with nTgHSP70 resulted in suppression of NO release on restimulation with nTgHSP70. Polymyxin B did not inhibit rTgHSP70- and nTgHSP70-induced tolerance of PMs from TLR4-deficient mice. Furthermore, PMs from WT mice increased suppressor of cytokine-signaling-1 (SOCS-1) expression after restimulation with rTgHSP70, while those from TLR4-deficient mice did not. Phosphorylation of JNK and I-κBα occurred in rTgHSP70-induced tolerance of PMs from TLR4-deficient mice, but not in that from WT mice. These data indicated that TgHSP70 signaling mechanisms were mediated by TLR2, MyD88, and IRAK4, but not by TLR4. On the other hand, signaling of TgHSP70-induced tolerance was mediated by TLR4, and the expression of SOCS-1 suppressed the TLR2 signaling pathway