The amebicidal activity of traditional anitiamoebic drug (emetine, carbasone, diodoquin, chloroquine, atabrine, chloramphenicol and tertracycline) and newly appeared chemicals(niridazole, metronidazole and No. 8603 substance) were assayed by in vitro experiment using five strains of human originated E, histolytica. The variety of amebicidal activity of drugs by the strains were discussed. Ranges of amoebicidal activity of traditional antiamoebic drugs kept almost similar titers of previous reports at the concentration; 1:5,000 to 1:20,000 with emetine hydrochloride, 1:10.000 to 1:20,000 with carbarsone, 1:8,000 to 1:16,000 with diodoquin, 1:50,000 with chloroquine, 1:1,000 to 1: 4,000 with atabrine ,1:1,000 to 1:2,000 with chloramphencol and 1:5,000 to 1:8,000 with tetracycline. The newly appeared chemicals showed higher amebicidal titres at the concentration; 1:500,000 to 1:5,000,000 with niridazole, 1:50,000 to 1:100,000 with metronidazol and 1:100,000 to 1:500,000 with No.8603 substance. Emetine, chloramphenicol and No. 8603 substance showed amebicidal activities at lower concentration to intestine originated amebae (YS 14, YS 15 and NAMRU II strain) than to liver originated amebae (YS 24 and YS 25 strain ), while carbarsone, chloroquine and metronidazole showed the activity at higher concentrations. Diodoquin showed lower amebicidal titres to trophozoite borne amebae (NAMRU II, YS 24 and YS 25 strain) than to cyst borne amebae(YS 14 and YS 15 strain), but niridazole showed converse results. The concentration of atabrine for amebicidal activity was not constant according to strains of the amoeba, but tetracycline showed almost settled titers.
parasitology-protozoa ; Entamoeba histolytica ; virulence ; in-vitro ; chemotherapy ; emetine ; carbasone ; diodoquin ; chloroquine ; atabrine ; chloramphenicol ; tertracycline ; niridazole ; metronidazole ; No. 8603 substance

This paper aims to examine the spread of paragonimiasis and the Japanese colonial government's response to it. To consolidate colonial rule, the Japanese colonial government needed medications to cure paragonimiasis. When Dr. Ikeda Masakata invented acid emetine to cure paragonimiasis in Manchuria in 1915, emetine treatment carried the risk of emetine poisoning such as fatigue, inappetence, heart failure, and death. Nonetheless, Japanese authorities forced clinical trials on human patients in colonial Korea during the 1910s and 1920s. The emetine poisoning accident in Yeongheung and Haenam counties in 1927 occurred in this context. The Japanese government concentrated on terminating an intermediary host instead of injecting emetine to repress endemic disease in Japan. However, the Japanese colonial government pushed ahead with emetine injections for healthy men through the Preliminary Bureau of Land Research in colonial Korea in 1917. This clinical trial simultaneously presented the effects and the side effects of emetine injection. Because of the danger emetine injections posed, the colonial government investigated only the actual condition of paragonimiasis, delaying the use of emetine injection. Kobayashi Harujiro(1884-1969), a leading zoologist and researcher of endemic disease for three decades in the Government General Hospital and Keijo Imperial University in colonial Korea, had used emetine while researching paragonimiasis, but he did not play a leading role in clinical trials with emetine injections, perhaps because he mainly researched the intermediary host. Government General Hospital and Keijo Imperial University therefore faced limitations that kept them from leading the research on endemic disease. As the health administration shifted the central colonial government to local colonial government, the local colonial government pressed ahead with emetine injections for Korean patients. Emetine poisoning had something to do with medical power's localization. Nevertheless, the central colonial government still supported emetine injections with funds from the national treasury. The emetine poisoning accident that occurred simultaneously in two different regions resulted from the Japanese colonial government's support. This accident represented the Japanese colonial rule's atrocity, its suppression of hygiene policies, and its disdain for colonial inhabitants. The colonial government sought to accumulate medical knowledge not to cure endemic disease, but to expand the Japanese Empire.
Clinical Trials as Topic/history ; Colonialism/*history ; Emetine/*history/poisoning/therapeutic use ; Endemic Diseases/*history ; History, 20th Century ; Human Experimentation/history ; Humans ; Japan ; Korea ; Male ; Paragonimiasis/drug therapy/*history

OBJECTIVE: Epigallocatethin gallate(EGCG) is a major green tea polyphenol and is known to have potent antioxidative and antiproliferative actions. This study is performed to investigate the antioxidative effect of EGCG on the various oxidative insults in mouse cerebral cortical cell cultures. METHODS: Mixed cortical cell cultures containing both neuron and glia prepared by plating fetal mice cortical cells on to an established glia of 24 well vessels. At 13-15 days in vitro, oxidative neuronal deaths were induced by the addition of oxidants into the cortical cultures. Iron ion(FeCl2), copper ion(CuCl2), sodium nitroprusside(SNP) and buthionine sulfoximine(BSO, a glutathione depletor) were used as oxidants. Cell death was assessed by LDH assay after microscopic examination. RESULTS: All four oxidants induced neuronal cell death associated with cell body swelling, which was markedly inhibited by Trolox(100muM), a vitamin E analog. EGCG(1-10muM) markedly inhibited the neuronal cell death induced by 20muM CuCl2, 1muM SNP, or 1mM BSO. Unexpectedly the neuronal cell death induced by 20muM FeCl2 was augmented by treatment with 1 or 3muM EGCG. EGCG itself induced concentration- and exposure time-dependent cell death at more than 30muM concentrations. EGCG(30, 100muM) injured not only neuronal cells but glial cells after 48 hour exposure. The EGCG-induced cytotoxicity was partially inhibited by protein synthesis inhibitors, cycloheximide(0.1 or 1mug/ml) and emetine (1mug/ml) or high potassium media(10 or 25mM) but was not affected by Trolox. CONCLUSION: These results suggest that the dual antioxidative-cytotoxic actions of EGCG are concentration-dependent and that the antioxidative aciton depends on the kind of oxidative insults, and that the EGCG-induced cytotoxicity be relevant to protein synthesis and/or membrane depolarization.
Animals ; Cell Culture Techniques* ; Cell Death ; Copper ; Emetine ; Glutathione ; Iron ; Membranes ; Mice ; Neuroglia ; Neurons ; Oxidants ; Potassium ; Protein Synthesis Inhibitors ; Sodium ; Tea ; Vitamin E ; Vitamins

Human Fasciola hepatica infection is a rare entity involving infestation of the liver and biliary tree with adult flukes, which can result in hepatitis, cirrhos is and biliary tract inflammation, obstruction and lithiasis. The patient had the typical diagnostic tetrad of fever, eosinophilic leukocytosis, tender hepatomegaly and fluke ova in the stools. Treatment consists of Emetine hydrochloride hydrochloride administration for hepatic involvement and common bile duct exploration for removal of flukes, with cholecystectomy for associated cholelithiasis. The combination of medical and surgical therapy can be expected to produce an arrest of this infection. The removed liver revealed eggs of the fasciola species in the intrahepatic bile duct. The clinical history, pathological findings and treatment of this case were described.
Adult ; Bile Ducts, Intrahepatic ; Biliary Tract ; Cholecystectomy ; Cholelithiasis ; Common Bile Duct ; Eggs ; Emetine ; Eosinophils ; Fasciola ; Fasciola hepatica ; Fascioliasis* ; Fever ; Hepatitis ; Hepatomegaly ; Humans* ; Inflammation ; Korea* ; Leukocytosis ; Lithiasis ; Liver* ; Ovum ; Trematoda

BACKGROUND: Apoptosis is a highly selective form of cell suicide with characteristic morphologieal and biochemical features, including chromatin condensation, formation of apoptotic bodies, and DNA fragmentation by the activation of endonucleases. Various cytokines and physical or chemical factors can provoke apoptotic changes in the skin. OBJECTIVE: We investigated the cytotoxic effects with epidermal cytokines and their combinations, K+ ionophores, protein synthesis inhibitor(emetine), inhibitor of endogenous endonuclease(aurintricarboxylic acid, ATA), sodium azide, and retinoic acid witp human epithelial tumor cell lines(A431 cells) to examine the degree of induction of apoptosis in the epidermal keratinocytes. METHODS: Induction of apoptosis was measured in cultured human keratinocytes, keratinocyte cell lines(A-431, HaCat, KB cells), cultured human melanocytes and malignant melanoma cell lines(SK-28, SK-30) using a mixture of ethidium bromide and acridine orange, DNA agarose gel electrophoresis and TUNEL staining. RESULTS: l. In the A-431 cells, (1 to a certain degree, the combination of IFN-gamma and TNF-alpha could only induce apoptosis. Q2 most of K+ ionophores were observed to induce necrosis rather than apoptosis. Q3 emetine, a protein synthesis blocker, was found to induce apoptosis in a dose-dependent pattern. Q4 sodium azide at a concentration of 1% .induced apoptosis rather than necrosis. Q5 retinoic acid inhibit the beuvericin induced apoptosis. 2. In human keratinocytes, Ql more resistant in the induction of apoptosis than any cultured keratinocyte cell lines p aurintricarboxylic acid(ATA)-an endonuclease inhibitor, could inhibit UV induced apoptosis 3. In human keratinocytes and cultured keratinocyte cell lines, c-PAF inhibit the beauvericin induced apoptosis. 4. Human melanocytes is very resistant for the induction of apoptosis by beauvericin. 5. In the melanocytes and melanoma cell lines, sodium azide and beauvericin induced necrosis rather than apoptosis. CONCLUSIONS: The epidermis is continuously exposed to toxic factors which might induce cell death. With the above results, the induction of appeared to be rather resistant, epidermal cell apoptosis which may reflect the existence of some endogenous protective mechanisms in the epidermis to survive at certain toxic environments; melanocytes showed high expression of bcl-2 protein which could play a role in endogenous defense against toxic environments of the epidermis.
Acridine Orange ; Apoptosis* ; Cell Death ; Cell Line ; Chromatin ; Cytokines ; DNA ; DNA Fragmentation ; Electrophoresis, Agar Gel ; Emetine ; Endonucleases ; Epidermis ; Ethidium ; Humans ; In Situ Nick-End Labeling ; Ionophores ; Keratinocytes ; Melanocytes ; Melanoma ; Necrosis ; Skin ; Sodium Azide ; Suicide ; Tretinoin ; Tumor Necrosis Factor-alpha