text:
Talk:Shishapangma

complete record of ascents to Shishapangma up to 2014
Name	F	Country	Date	Route	Remark

1	CHANG Chun-yen		China	2.5.64	NE Face - Chinese traverse

2	CHEN San		China	2.5.64	NE Face - Chinese traverse

3	CHENG Tien-liang		China	2.5.64	NE Face - Chinese traverse

4	DOJI CHN		Tibet	2.5.64	NE Face - Chinese traverse

5	HSU Ching		China	2.5.64	NE Face - Chinese traverse

6	MIGMAR TRASHI		Tibet	2.5.64	NE Face - Chinese traverse

7	SODNAM DOJI		Tibet	2.5.64	NE Face - Chinese traverse

8	WANG Fu-Zhou		China	2.5.64	NE Face - Chinese traverse

9	WU Tsung-yue		China	2.5.64	NE Face - Chinese traverse

10	YONTEN		Tibet	2.5.64	NE Face - Chinese traverse

11	DACHER Michael (Michel)		Bavaria/D	7.5.80	NE Face - Chinese traverse

12	SCHAFFERT Wolfgang		GER	7.5.80	NE Face - Chinese traverse

13	STURM Günter		Bavaria/D	7.5.80	NE Face - Chinese traverse

14	ZINTL Friedrich (Fritz)		GER	7.5.80	NE Face - Chinese traverse

15	HUPFAUER Siegfried (Sigi)		Bavaria/D	12.5.80	NE Face - Chinese traverse

16	STURM Manfred		GER	12.5.80	NE Face - Chinese traverse

17	OBOJES Egon A		Tirol	13.10.80	NE Face - Central traverse to E Ridge

18	PUTZ Ewald A		Austria	13.10.80	NE Face - Central traverse to E Ridge

19	JIABU (GYALBU)		Tibet	30.4.81	NE Face - Chinese traverse	1

20	RINGQING PINGCUO		Tibet	30.4.81	NE Face - Chinese traverse

21	TABEI (b ISHIBASHI) Junko	♀	JPN	30.4.81	NE Face - Chinese traverse

22	MESSNER Reinhold		S-Tirol/I	28.5.81	NE Face - traverse to W Ridge

23	MUTSCHLECHNER Gottfried (Friedl)		S-Tirol/I	28.5.81	NE Face - traverse to W Ridge

24	BAXTER-JONES Roger Gregory		England	28.5.82	SW Face, Central Couloir

25	MacINTYRE Alex		UK	28.5.82	SW Face, Central Couloir

26	SCOTT Douglas Keith (Doug)		England	28.5.82	SW Face, Central Couloir

27	SCHUM Ulrich		GER	29.4.83	NE Face - Chinese traverse

28	WALTER Josef		GER	29.4.83	NE Face - Chinese traverse

29	WALTER Marianne	♀	GER	29.4.83	NE Face - Chinese traverse

30	BROWNING Michael		USA	30.9.83	NE Face - Chinese traverse

31	PIZZO Christopher		USA	30.9.83	NE Face - Chinese traverse

32	PORZAK Glenn E.		USA	30.9.83	NE Face - Chinese traverse

33	HOWE David E.		USA	6.5.84	NE Face - Chinese traverse

34	JENKINS Mark David		USA	6.5.84	NE Face - Chinese traverse

35	KELLEY Douglas A.		USA	6.5.84	NE Face - Chinese traverse

36	WINGERT Michael		USA	6.5.84	NE Face - Chinese traverse

37	CREER Steve		USA	8.5.84	NE Face - Chinese traverse

38	LEHNER Michael		USA	8.5.84	NE Face - Chinese traverse

39	GASSLER Oswald A		Tirol	10.5.85	NE Face - Chinese traverse

40	SCHAUSBERGER Leopold A		Austria	10.5.85	NE Face - Chinese traverse

41	WÖRGÖTTER Peter A		Salzburg/Aut	10.5.85	NE Face - Chinese traverse

42	HEINZEL Gottfried A		Austria	12.5.85	NE Face - Chinese traverse

43	KENDLER Balthasar A		Salzburg/Aut	12.5.85	NE Face - Chinese traverse

44	SCHILCHER Thomas A		Austria	12.5.85	NE Face - Chinese traverse	1

45	VEDANI Angelo		Suisse	12.5.85	NE Face - Chinese traverse

46	WAGNER Helmut		Tirol/Aut	12.5.85	NE Face - Chinese traverse

47	WANGELER Josef		Suisse	12.5.85	NE Face - Chinese traverse

48	WETTSTEIN Max		Suisse	12.5.85	NE Face - Chinese traverse

49	DE MARCHI Giuliano		ITA	16.5.85	NE Face - Chinese traverse

50	KARNER Leopold		Styria/Aut	19.5.85	NE Face - Chinese traverse

51	SCHELL Hanns 		Styria/Aut	19.5.85	NE Face - Chinese traverse

52	SCHILCHER Thomas		Austria	19.5.85	NE Face - Chinese traverse	2

53	LEUPRECHT Michael		Tirol/Aut	20.9.86	N Ridge - C Peak - W Ridge

54	OBERAUER Josef (Sepp)		Tirol/Aut	20.9.86	N Ridge - C Peak - W Ridge

55	PERRY Michael		NZL	20.5.87	NE Face - Chinese traverse

56	WHETU Mark		Maori/NZL	20.5.87	NE Face - Chinese traverse

57	AVILA Elsa	♀	MEX	18.9.87	N Ridge - C Peak - W Ridge

58	CARSOLIO Carlos		MEX	18.9.87	N Ridge - C Peak - W Ridge

59	HAJZER Artur Henryk		POL	18.9.87	W Ridge

60	KUKUCZKA Jerzy		POL	18.9.87	W Ridge

61	NAVARRETE Ramiro		ECU	18.9.87	N Ridge - C Peak - W Ridge

62	RUTKIEWICZ/BŁASZKIEWICZ Wanda	♀	POL	18.9.87	N Ridge - C Peak - W Ridge

63	WARECKI Ryszard		POL	18.9.87	N Ridge - C Peak - W Ridge

64	HINKES Alan		England	19.9.87	C Couloir of N Face, Central-Peak

65	UNTCH Steven Donald Frederick (Steve)		USA	19.9.87	C Couloir of N Face, Central-Peak

66	FISCHBACH Tilman		GER	13.5.88	N Ridge - C Peak - W Ridge

67	GÜRTLER Klaus		Tirol/Aut	13.5.88	N Ridge - C Peak - W Ridge

68	KONZERT Peter		Austria	13.5.88	N Ridge - C Peak - W Ridge

69	KULLMANN Bernd		GER	13.5.88	NE Face - Chinese traverse

70	METZGER Adolf		GER	14.5.88	NE Face - Chinese traverse

71	OG Herta	♀	GER	14.5.88	NE Face - Chinese traverse

72	SCHUHMANN Klaus		GER	14.5.88	NE Face - Chinese traverse

73	BÄRNTHALER Hans		Styria/Aut	17.5.88	NE Face - Chinese traverse

74	HOCHHOLZER Thomas		GER	17.5.88	NE Face - Chinese traverse

75	KUNZENDORF Wolfgang		GER	17.5.88	NE Face - Chinese traverse

76	SCHÜTZ Jürgen		GER	17.5.88	NE Face - Chinese traverse

77	THOMANN Dieter		GER	17.5.88	NE Face - Chinese traverse

78	BÉRHAULT Patrick		F	5.9.88	NE Face - Chinese traverse

79	DE STEFANI Fausto		ITA	5.9.88	NE Face - Chinese traverse

80	MARTINI Sergio		ITA	5.9.88	NE Face - Chinese traverse

81	DAIDOLA Giorgio		ITA	6.9.88	NE Face - Chinese traverse

82	GIVOIS Didier		F	6.9.88	NE Face - Chinese traverse

83	NEGRI Pino		ITA	6.9.88	NE Face - Chinese traverse

84	SAEGUSA Teruo		JPN	24.10.88	NE Face - Chinese traverse

85	YAMADA Noboru		JPN	24.10.88	NE Face - Chinese traverse

86	YAMAMOTO Atsushi		JPN	24.10.88	NE Face - Chinese traverse

87	SUZUKI Kiyohiko		JPN	16.11.88	NE Face - Chinese traverse

88	TAKAMURA Sinji		JPN	16.11.88	NE Face - Chinese traverse

89	TSUJI Yoshiyuki		JPN	16.4.89	NE Face - Chinese traverse

90	KOZJEK Pavle		SLO	19.10.89	SW Face, Central Buttress

91	ŠTREMFELJ Andrej		SLO	19.10.89	SW Face, Central Buttress

92	BENCE Filip (Ta črn)		SLO	20.10.89	SW Face (Right Part) - SE Ridge

93	GROŠELJ Viktor (Viki)		SLO	20.10.89	SW Face (Right Part) - SE Ridge

94	FRIES Elmar		GER	12.5.90	NE Face - Chinese traverse

95	NEUHAUSER Johann		Austria	12.5.90	NE Face - Chinese traverse

96	EXPÓSITO Pedro		Aragon/Esp	13.10.90	NE Face - Chinese traverse

97	GAN Francisco (Curro)		Catalan/Esp	13.10.90	NE Face - Chinese traverse

98	MARTÍNEZ Joan		Catalan/Esp	13.10.90	NE Face - Chinese traverse

99	PÉREZ Francisco		Andalus/Esp	13.10.90	NE Face - Chinese traverse

100	SANTAEUFEMIA Roberto		Basque/Esp	13.10.90	NE Face - Chinese traverse

101	VIDAL Miguel Ángel		Castile-Leon/Esp	13.10.90	NE Face - Chinese traverse

102	DÖRRICH Ottilie	♀	GER	20.5.91	NE Face - Chinese traverse

103	FRITSCHE Theo		Vorarlbg/Aut	20.5.91	NE Face - Chinese traverse

104	HÄRTER Günther		GER	20.5.91	NE Face - Chinese traverse

105	HECHER Kurt		Kärnten/Aut	20.5.91	NE Face - Chinese traverse

106	PORSCHE Dieter Albin		GER	20.5.91	NE Face - Chinese traverse

107	SCHNUTT Herwig		Styria/Aut	20.5.91	NE Face - Chinese traverse

108	KIM Chang-Seon		S-Korea	8.10.91	SW Face, Central Couloir

109	KIM Jae-Soo		S-Korea	8.10.91	SW Face, Central Couloir

110	CADIACH Òscar		Catalan/Esp	4.10.93	SW Face, Central Couloir

111	DE LA MATTA Manel		Catalan/Esp	4.10.93	SW Face, Central Couloir

112	MAUDUIT Chantal	♀	F	4.10.93	SW Face, Central Couloir

113	BIANCHI Marco		ITA	6.10.93	SW Face (Right Part) - SE Ridge

114	PUSTELNIK Piotr Czeslaw (Pusty)		POL	6.10.93	SW Face (Right Part) - SE Ridge

115	WIELICKI Krzysztof		POL	7.10.93	SW Face, Right Hand Couloir

116	AKBU (AKEBU)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

117	DACHUNG (DAQIONG)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

118	DAQIMI (DA CHIMYI)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

119	JIABU (GYALBU)		Tibet	7.5.94	N Ridge - C Peak - W Ridge	2

120	LUOZE (LODUE)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

121	PEMBA TASHI (BIANBA ZAXI) I		Tibet	7.5.94	N Ridge - C Peak - W Ridge

122	RENA (REN NA)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

123	TSERING DORJE I (CERIN DUOJI)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

124	WANGJIA (WANGYAL)		Tibet	7.5.94	N Ridge - C Peak - W Ridge

125	KIRSCHMER Jakob		GER	28.5.94	N Ridge - C Peak - W Ridge

126	KEKUS Nikola		England	4.10.94	N Ridge - C Peak - W Ridge

127	LORETAN Erhard		Suisse	29.4.95	N Ridge - C Peak - W Ridge

128	RATTEIT Rodja		GER	12.5.95	N Ridge - C Peak - W Ridge

129	KOTRONAROS Panagiotis		GRE	13.5.95	N Ridge - C Peak - W Ridge

130	SONAM DENDU (SONA DENDU) Sherpa		NEP	13.5.95	N Ridge - C Peak - W Ridge

131	JOOS Norbert (Noppa)		Suisse	1.5.96	N Ridge - C Peak - W Ridge

132	SLUKA Štefan		SVK	1.5.96	NE Face - Chinese traverse

133	ŠPERKA Peter		SVK	1.5.96	NE Face - Chinese traverse

134	HASLER Bruno		Suisse	21.5.96	NE Face - Chinese traverse

135	ZINSLI Christian		Suisse	21.5.96	NE Face - Chinese traverse

136	GUGGEMOS Peter		Bavaria/D	30.5.96	NE Face - Chinese traverse

137	SCHNEIDER Manuel		GER	30.5.96	NE Face - Chinese traverse

138	BEREZIARTUA Jesús (Josu)		Basque/Esp	11.10.96	SW Face, Central Couloir

139	IÑURRATEGI Alberto		Basque/Esp	11.10.96	SW Face, Central Couloir

140	IÑURRATEGI Félix		Basque/Esp	11.10.96	SW Face, Central Couloir

141	BRILL Peter		GER	24.5.97	NE Face - Chinese traverse

142	DUJMOVITS Ralf		GER	24.5.97	NE Face - Chinese traverse	1

143	HUB Karl		GER	24.5.97	NE Face - Chinese traverse

144	NEUHUBER Alois		Austria	24.5.97	NE Face - Chinese traverse

145	OSTERBAUER Gerhard		Vienna/Aut	24.5.97	NE Face - Chinese traverse

146	PRASICEK Franz		Austria	24.5.97	NE Face - Chinese traverse

147	ANDRES Stefan		S-Tirol	6.5.98	NE Face - Chinese traverse

148	KUNTNER Christian		S-Tirol	6.5.98	NE Face - Chinese traverse

149	BLANC Abele		Aosta/Ita	14.5.98	N Ridge - C Peak - W Ridge

150	CAMANDONA Marco		ITA	14.5.98	N Ridge - C Peak - W Ridge

151	NICLEVICZ Waldemar		BRA	14.5.98	N Ridge - C Peak - W Ridge

152	OIARZABAL Juan Eusebio (Juanito)		Basque-Álava/Esp	10.10.98	SW Face, Central Couloir

153	STANGL Christian		Styria/Aut	10.10.98	SW Face, Central Couloir

154	KEREJETA Ignacio (Iñaki)		Basque-Álava/Esp	11.10.98	SW Face, Central Couloir

155	BENET Romaniaano		ITA	12.5.99	NE Face - Chinese traverse

156	MEROI Nives	♀	ITA	12.5.99	NE Face - Chinese traverse

157	FUKUMOTO Masashi		JPN	29.10.99	NE Face - Chinese traverse

158	GOTO Fumiaki		JPN	29.10.99	NE Face - Chinese traverse

159	HOSHINO Ryushi		JPN	29.10.99	NE Face - Chinese traverse

160	KENMOCHI Noriyuki		JPN	29.10.99	NE Face - Chinese traverse	1

161	NAZUKA Hideji		JPN	29.10.99	NE Face - Chinese traverse

162	KHADEM Davoud		IRN	28.5.00	N Ridge - C Peak - W Ridge

163	MEHDIZADEH Akbar		IRN	28.5.00	N Ridge - C Peak - W Ridge

164	ORAZ Mohammad		IRN	28.5.00	N Ridge - C Peak - W Ridge

165	KANG Seong-Gyu		S-Korea	2.10.00	SW Face, Central Couloir

166	OH Hee-Jun		S-Korea	2.10.00	SW Face, Central Couloir

167	PARK Young-Seok		S-Korea	2.10.00	SW Face, Central Couloir

168	SHERAP JANGBU (SERAP JANGBU)		NEP	2.10.00	SW Face, Central Couloir

169	KWON Soon-Jae		S-Korea	5.10.00	SW Face, Central Couloir

170	LEE Gin-Kun		S-Korea	5.10.00	SW Face, Central Couloir

171	LEE Hyun-Jo		S-Korea	5.10.00	SW Face, Central Couloir

172	BOSKOFF (b FELD) Christine Joyce	♀	USA	10.10.00	SW Face, Central Couloir

173	FOWLER Charles (Charlie)		USA	10.10.00	SW Face, Central Couloir

174	GUSTAFSSON Veikka		SF	30.4.01	N Ridge - C Peak - W Ridge

175	VIESTURS Edmund (Ed)		USA	30.4.01	N Ridge - C Peak - W Ridge

176	ANG BABU (JIMBA ZANGBU)		NEP	21.9.01	SW Face, Central Couloir

177	HAN Wang-Yong		S-Korea	21.9.01	SW Face, Central Couloir

178	KIM Joo-Hyung		S-Korea	21.9.01	SW Face, Central Couloir

179	KOO Eun-Soo		S-Korea	21.9.01	SW Face, Central Couloir

180	PARK Mu-Taek		S-Korea	21.9.01	SW Face, Central Couloir

181	RA Kwan-Ju		S-Korea	21.9.01	SW Face, Central Couloir

182	UM Hong-Gil		S-Korea	21.9.01	SW Face, Central Couloir

183	KIM Woong-Sik		S-Korea	22.9.01	SW Face, Central Couloir

184	MINGMA I Sherpa		NEP	22.9.01	SW Face, Central Couloir

185	GEX Nicolas		Suisse	24.9.01	SW Face, Central Couloir

186	REICHEN Jakob (Köbi)		Suisse	24.9.01	SW Face, Central Couloir

187	RODUIT Olivier		Suisse	24.9.01	SW Face, Central Couloir

188	WARNER Christopher Bernard (Chris)		USA	24.9.01	SW Face, Central Couloir

189	KHOO Swee-Chiow		SIN (?)	28.9.01	SW Face, Central Couloir

190	SHAW Christopher		USA	28.9.01	SW Face, Central Couloir

191	KANG Yeon-Ryong		S-Korea	5.5.02	SW Face, West Central Buttress

192	PARK Jung-Hun		S-Korea	5.5.02	SW Face, West Central Buttress

193	BOGOMOLOV Sergei		RUS	24.5.02	NE Face - Lower traverse - E Ridge

194	OLEYNIK Vladimir		RUS	24.5.02	NE Face - Lower traverse - E Ridge

195	HUMAR Tomaž		SLO	25.10.02	N Ridge - C Peak - W Ridge

196	PIVTSOV Vassili (Vaso)		KAZ	25.10.02	N Ridge - C Peak - W Ridge

197	RASPOPOV Aleksei		KAZ	25.10.02	N Ridge - C Peak - W Ridge

198	URUBKO Denis		KAZ	25.10.02	N Ridge - C Peak - W Ridge

199	ZHUMAYEV Maksut (Max)		KAZ	25.10.02	N Ridge - C Peak - W Ridge

200	BRILL Richard		GER	8.5.04	NE Face - Chinese traverse

201	BRUNI Hans		Suisse	8.5.04	NE Face - Chinese traverse

202	DUBACH Hanspeter		Suisse	8.5.04	NE Face - Chinese traverse

203	GOLTZ Uwe Johannes (Gianni)		Suisse	8.5.04	NE Face - Chinese traverse

204	ROTH Hanspeter		Suisse	8.5.04	NE Face - Chinese traverse

205	ABEGGLEN Andreas		Suisse	14.5.04	NE Face - Chinese traverse

206	GÜRTLER Paul		Tirol	14.5.04	NE Face - Chinese traverse

207	JACOMET Ervin		Suisse	14.5.04	NE Face - Chinese traverse

208	KAUFMANN Johann		Suisse	14.5.04	NE Face - Chinese traverse

209	KECK Stephan		Tirol	14.5.04	NE Face - Chinese traverse

210	VON ROTZ Josef (Sepp)		Suisse	14.5.04	NE Face - Chinese traverse

211	EMMENEGGER Patrik Klaus		Suisse	16.5.04	NE Face - Chinese traverse

212	FALCH Josef		Tirol	16.5.04	NE Face - Chinese traverse

213	FELDER Josef (Sepp)		Vorarlbg/Aut	16.5.04	NE Face - Chinese traverse

214	FURGER Karl		Suisse	16.5.04	NE Face - Chinese traverse

215	LESKAUSKAS Mindaugas		LIT	16.5.04	NE Face - Chinese traverse

216	MITENJEN (MINGMA) Sherpa		NEP	16.5.04	NE Face - Chinese traverse

217	NGIMA DORCHI Sherpa		NEP	16.5.04	NE Face - Chinese traverse

218	NGIMA THENDUK Sherpa		NEP	16.5.04	NE Face - Chinese traverse

219	SUTTERLÜTY Martin (Prinz)		Vorarlbg/Aut	16.5.04	NE Face - Chinese traverse

220	VALLOTON Josette	♀	Suisse	16.5.04	NE Face - Chinese traverse

221	HRUBÝ Zdeněk		CZE	9.10.04	SW Face, Central Couloir

222	JAROŠ Radek		CZE	9.10.04	SW Face, Central Couloir

223	MAŠEK Petr (Miska)		CZE	9.10.04	SW Face, Central Couloir

224	MINAŘÍK Martin		CZE	9.10.04	SW Face, Central Couloir

225	RIBAS Oriol		AND	10.10.04	SW Face, Central Couloir

226	ROSELL Ramón		AND	10.10.04	SW Face, Central Couloir

227	SAGASTE Santiago		Aragon/Esp	10.10.04	SW Face, Central Couloir

228	VALLEJO Iván		ECU	10.10.04	SW Face, Central Couloir

229	LAFAILLE Jean-Christophe		F	11.12.04	SW Face, Right Hand to Central Couloir

230	MORAWSKI Piotr		POL	14.1.05	SW Face (Right Part) - SE Ridge

231	MORO Simone		ITA	14.1.05	SW Face (Right Part) - SE Ridge

232	GÖSCHL Gerfried		Styria/Aut	3.5.05	NE Face - Chinese traverse

233	DUJMOVITS Ralf		GER	7.5.05	SW Face, Central Couloir	2

234	KALTENBRUNNER Gerlinde	♀	Austria	7.5.05	SW Face, Central Couloir

235	TAKEUCHI Hirotaka		JPN	7.5.05	SW Face, Central Couloir

236	BRUN Nicolas		F	4.10.05	SW Face, Central Couloir

237	EGOCHEAGA Jorge		Asturia/Esp	4.10.05	SW Face, Central Couloir

238	LATORRE Fernando (Ferrán)		Catalan/Esp	4.10.05	SW Face, Central Couloir

239	TAMAYO José Carlos		Basque/Esp	4.10.05	SW Face, Central Couloir

240	URBAN Jean-Noël		F	4.10.05	SW Face, Central Couloir

241	VALLEJO Juan		Basque-Álava/Esp	4.10.05	SW Face, Central Couloir

242	CONFORTOLA Marco		ITA	9.5.06	NE Face - Chinese traverse

243	ENZIO Michele		ITA	9.5.06	NE Face - Chinese traverse

244	FERNÁNDEZ-VIVANCOS Fernando		Andalus/Esp	9.5.06	NE Face - Chinese traverse

245	GOBBI Christian		ITA	9.5.06	NE Face - Chinese traverse

246	GOGER Johann (Hans)		Burgenld/Aut	9.5.06	NE Face - Chinese traverse

247	MARUNA Anita	♀	Austria	9.5.06	NE Face - Chinese traverse

248	MONDINELLI Silvio (Gnaro)		ITA	9.5.06	NE Face - Chinese traverse

249	RODRÍGUEZ Julian		Basque/Esp	9.5.06	NE Face - Chinese traverse

250	TRÅ Jarle		NOR	10.5.06	NE Face - Chinese traverse

251	AMANO Kazuaki		JPN	18.5.06	N Ridge - C Peak - W Ridge

252	KATO Yoshinobu		JPN	18.5.06	N Ridge - C Peak - W Ridge

253	JANG Jung-Kyu		S-Korea	3.10.06	SW Face, Central Couloir

254	KIM Hong-Bin		S-Korea	3.10.06	SW Face, Central Couloir

255	OCHOA DE OLZA Ignacio (Iñaki)	♀	Basque/Esp	3.10.06	NE Face - Lower to Central traverse - E Ridge

256	OH Eun-Sun		S-Korea	3.10.06	SW Face, Central Couloir

257	THILEN Sherpa		NEP	3.10.06	SW Face, Central Couloir

258	FUJIKAWA Katsuhito		JPN	9.10.06	NE Face - Chinese traverse

259	GÁLVEZ Jorge (Koki)		PER	9.10.06	NE Face - Chinese traverse

260	HIDALGO Richard Leopoldo		PER	9.10.06	NE Face - Chinese traverse

261	KENMOCHI Noriyuki		JPN	9.10.06	NE Face - Chinese traverse	2

262	LA TERRA Simone		ITA	9.10.06	NE Face - Chinese traverse

263	SENDA Atsushi		JPN	9.10.06	NE Face - Chinese traverse

264	TANABE Osamu		JPN	9.10.06	NE Face - Chinese traverse

265	YAMAGUCHI Takahiro		JPN	9.10.06	NE Face - Chinese traverse

266	YAMAMOTO Toshio (2)		JPN	9.10.06	NE Face - Chinese traverse

267	CARVALHO Bruno		POR	31.10.06	NE Face - Chinese traverse

268	GARCIA João		POR	31.10.06	NE Face - Chinese traverse

269	NURU (a) Sherpa		NEP	31.10.06	NE Face - Chinese traverse

270	ROSADO Rui		POR	31.10.06	NE Face - Chinese traverse

271	KOPOLD Jozef (Dodo)		SVK	24.4.07	SW Face, Central Couloir

272	HOFER Hansjörg		S-Tirol	15.5.07	N Ridge - C Peak - W Ridge

273	MERKEL Thomas (Tom)		Rheinland/D	15.5.07	N Ridge - C Peak - W Ridge

274	PIRCHER Rainer		GER	15.5.07	N Ridge - C Peak - W Ridge

275	CEVALLOS Alfredo		ARG	4.10.07	SW Face, Central Couloir

276	SACCHI Federico		ARG	4.10.07	SW Face, Central Couloir

277	GO Mi-Sun (Mi-Young)	♀	S-Korea	5.10.07	SW Face, Central Couloir

278	JUMIK BHOTE		Bhutan/Nep	5.10.07	SW Face, Central Couloir

279	KIM Jae-Soo		S-Korea	5.10.07	SW Face, Central Couloir

280	TARKE Sherpa		NEP	5.10.07	SW Face, Central Couloir

281	TSHERING JANGBU Sherpa		NEP	5.10.07	SW Face, Central Couloir

282	LASA José Ramón (Koke)		Basque/Esp	8.10.07	SW Face, Central Couloir

283	MORÁVEK Josef (Pepino)		CZE	8.10.07	SW Face, Central Couloir

284	TXIKON Jon Alexander (Alex)		Basque/Esp	8.10.07	SW Face, Central Couloir

285	ZAMBALDI Andrea		ITA	2.10.08	N Ridge - C Peak - W Ridge

286	MONTOLLI Andrea		ITA	3.10.08	N Ridge - C Peak - W Ridge

287	LOCK Andrew		AUS	2.10.09	NE Face - Lower to Central traverse - E Ridge

288	WARD Neil		Wales	2.10.09	NE Face - Lower to Central traverse - E Ridge

289	BENEDETTI Renzo		ITA	17.5.10	NE Face - Lower to Central traverse - E Ridge

290	BIBAS GURUNG Sherpa		Gurung/Nep	17.5.10	NE Face - Lower to Central traverse - E Ridge

291	COMPAGNONI Michele		ITA	17.5.10	NE Face - Lower to Central traverse - E Ridge

292	GARCÍA María Isabel (Isa)	♀	Castile-Leon/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

293	GIBERNAU Jaume		Catalan/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

294	GYALZEN II Sherpa		NEP	17.5.10	NE Face - Lower to Central traverse - E Ridge

295	IZAGUIRRE Asier		Basque/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

296	KAMI III Sherpa		NEP	17.5.10	NE Face - Lower to Central traverse - E Ridge

297	KONDO Kazuyoshi		JPN	17.5.10	NE Face - Lower to Central traverse - E Ridge

298	MADARIAGA Juan Ramón (Juanra)		Basque/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

299	MINGMA THINDUK II Sherpa		NEP	17.5.10	NE Face - Lower to Central traverse - E Ridge

300	ORVIZ Ignacio (Nacho), José		Asturia/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

301	PANZERI Mario Luciano		ITA	17.5.10	NE Face - Lower to Central traverse - E Ridge

302	PASABAN Edurne	♀	Basque/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

303	PASANG NURU b Sherpa		NEP	17.5.10	NE Face - Lower to Central traverse - E Ridge

304	PASANG TENDI a Sherpa		NEP	17.5.10	NE Face - Lower to Central traverse - E Ridge

305	RODRIGO Roberto		Basque/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

306	SALAZAR Jorge Antonio		MEX	17.5.10	NE Face - Lower to Central traverse - E Ridge

307	TXIKON Jon Alexander (Alex)		Basque/Esp	17.5.10	NE Face - Lower to Central traverse - E Ridge

308	KIM Chang-Ho		S-Korea	14.10.10	SW Face, Central Couloir

309	SEO Sung-Ho		S-Korea	14.10.10	SW Face, Central Couloir

310	STECK Ulrich (Ueli)		Suisse	17.4.11	SW Face, Girone Corridor, Right Hand Couloir	disputed!

311	KIM Mi-Gon		S-Korea	8.10.11	SW Face, Central Couloir

312	SANU Sherpa		NEP	8.10.11	SW Face, Central Couloir

313	CHHANG DAWA Sherpa		NEP	30.4.13	NE Face - Lower to Central traverse - E Ridge

314	FıNDıK Tunç		TUR	30.4.13	NE Face - Lower to Central traverse - E Ridge

315	GAVAN Alexandru Costin (Alex)		Romania	30.4.13	NE Face - Lower to Central traverse - E Ridge

316	HAUER Rupert Arnold		Salzburg/Aut	30.4.13	NE Face - Lower to Central traverse - E Ridge

317	LÄMMLE Thomas		GER	30.4.13	NE Face - Lower to Central traverse - E Ridge

318	MINGMA THINDUK II Sherpa		NEP	30.4.13	NE Face - Lower to Central traverse - E Ridge

319	NIMA DORJE II (BOKA LAMA) Sherpa		NEP	30.4.13	NE Face - Lower to Central traverse - E Ridge

320	QUINTERO Santiago		ECU	30.4.13	NE Face - Lower to Central traverse - E Ridge

321	STITZINGER Luis		GER	30.4.13	NE Face - Lower to Central traverse - E Ridge

322	VON MELLE Alix Christine Dorothée	♀	GER	30.4.13	NE Face - Lower to Central traverse - E Ridge

323	BARGIEL Andrzej		POL	2.10.13	NE Face - Chinese traverse

324	COLIBǍŞANU Horia		Romania	30.4.14	NE Face - Lower to Central traverse - E Ridge

325	HÁMOR Peter		SVK	30.4.14	NE Face - Lower to Central traverse - E Ridge

326	IONESCU Justin, George		Romania	30.4.14	NE Face - Lower to Central traverse - E Ridge

327	GHEICHISAZ Azim		Persia/IRI	1.5.14	NE Face - Lower to Central traverse - E Ridge

328	BLETTON Antoine		F	14.5.14	SW Face, Central Couloir

329	BONNIOT Max		F	14.5.14	SW Face, Central Couloir

330	MOATTI Sébastien		F	14.5.14	SW Face, Central Couloir

331	RATEL Sébastien		F	14.5.14	SW Face, Central Couloir

col1 #, col2 Name, col3 female (17), col4 country, col5 date, col6 route taken.

Source: .pdf by © 2019 E. Jurgalski Shishapangma Ascents https://www.8000ers.com/cms/en/download.html?func=fileinfo&id=164 free for download.

Hope this is interesting enough for you!

Best wishes, sincerely, Wolfgang. 2A02:8071:287:95E0:E155:2CBB:19C6:5B7C (talk) 20:59, 29 November 2023 (UTC)

 * Thanks, Wolfgang, this is interesting in deed! 2003:E9:EF1B:53C:7C07:E4A8:55B4:9456 (talk) 10:17, 11 July 2024 (UTC)

title: Talk:Shishapangma


text: Talk:Walvisteuthis

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Talk:Walvisteuthis


text:
Talk:Geringoso

What about syllables that end in consonants, like este -> does it become espestepe or esptepe or epestepe or what? Nohat 20:32, 2004 May 2 (UTC)

 * I asked a Colombian friend, and he says este -> epestepe, but my discussions revealed a new question: what about diphthongs? Does voy become vopoy, voypoy, voypi, vopoipi, or what?

 * This game seems to go by the name "Jeringonza" in Colombia. Nohat 01:04, 2004 May 3 (UTC)

Don't know specifically of any rule, but I do know that in talking, "Sos un..." becomes -> "Sospo unpu" Wampa_Jabba

I added a line to the article stating that this game is known as "Jerigonza" (NOTE: not "Jeringonza" as someone else said). The word "Jerigonza" actually appears in the RAE (Royal Academy of the Spanish Language), unlike "Jeringonza" and even "Geringoso", this article's original word, which DO NOT appear and, therefore, seem not to be accepted as official words in Spanish.

Question: I made the "Jerigonza" word into a link, but it doesn't point anywhere. Where should it point?

title: Talk:Geringoso


text:
King Faisal Mosque

King Faisal Mosque may refer to:

 * Faisal Mosque in Islamabad, Pakistan
 * King Faisal Mosque, Sharjah, United Arab Emirates

title: King Faisal Mosque


text:
Sugama Sangeetha

Sugama Sangeetha, a variety of Bhavageethe, is an Indian musical genre in which poetry in the Kannada language is set to music. It gained recognition with the work of P. Kalinga Rao in the mid -20th century. Mysore Ananthaswamy and C. Aswath developed the form further in the 1960s and 1970s.

Origin and development
It is unclear when exactly Bhavageethe started but in 1920s and 30s there were many attempts to set tunes to poetry. By the 1950s it started taking a more defined shape and a highly talented musician – P. Kalinga Rao – was instrumental in spreading this art form. He set tunes to the poems of many famous Navodaya poets, and gave performances on All India Radio as well as public gatherings. The art form started gaining popularity through his rendering of Udayavaagali Namma Cheluvu Kannada Naadu, Yaaru Hitavaru Ninage, Anathadim Digantadim, Baarayya Beladingale, Brahma Ninge Jodistheeni etc., He laid the foundation of Sugama Sangeetha and hence is considered to be the father of this form.

The 60s and 70s saw many emerging musicians contributing to this field. H.R.Leelavathi, Padmacharan, H. K. Narayana in South Karnataka and Balappa Hukkeri in North Karnataka played a significant role in popularising the art across Karnataka. They also contributed to the field through their own compositions.

The next major personality in the field was Mysore Ananthaswamy. Till then, though there were a lot of compositions, they remained as more or less a subset of classical music from the musical perspective. It was Ananthaswamy who could think out of the box. He not only crossed the barrier of classical music, but was instrumental in adding its own subtleties to Bhaavageethe. With instrumentation also taking different shape by that time, he introduced a number of changes to orchestration. By that time, Bhavageethe was quite popular and businessmen began to publish it in cassette form. With that, 'Nithyotsava' became the first Bhavageethe album to be released. There were a lot of popular albums to his credit. 'Nithyotsava', 'Bhava Sangama', 'Minchu', 'Rathnana Padagalu' to mention a few.

Another young and dynamic talent emerged in the 70s: C. Aswath. Highly talented and a great visionary, his way of blending the lyrical and musical dynamics was hard to match. His way of rendering a song, with emphasis on lyrical dynamics and word power was distinctive. He also brought about a number of changes to the art. Dramatic elements, virtual picturization and other innovations could be observed in abundance in his compositions. He was instrumental in making Shishunala Sharif's poems popular across Karnataka. His popular albums are 'Mysooru Mallige', 'Shishunala Sharif Sahebara Geethegalu', 'Chaitra', 'Kannadave Satya' etc.,

P.Kalinga Rao, Mysore Ananthaswamy and C.Aswath are considered to be the trinity of Sugama Sangeetha. The mid 70s to mid 90s were probably the golden age since, in this period, the major exponents Ananthaswamy and Aswath were at the peak of their careers. The art form had matured enough to be considered an independent genre, and it started adding its own theories through experiments, while commercialisation due to increasing popularity and subsequent dilution of the art had not yet started.

Notable contributors
Many musicians have been successful in popularising Sugama Sangeetha through their compositions or singing, including:

Composers
P.Kalinga Rao, Mysore Ananthaswamy, C.Aswath, H. K. Narayana, Padmacharan, H.R.Leelavathi, Baalappa Hukkeri, Madikeri Nagendra, Raju Ananthaswamy, N.S.Prasad, B.K.Chandrashekar, B.V.Srinivas, Sunitha Ananthaswamy, Jayashree Arvind, Praveen D Rao, Pravin Godkhindi, M.D.Pallavi, Archana Udupa, Chidambara Kalamanji, Mahesh Mahadev, Upasana Mohan, Vasantha Kanakapur, Gartikere Raganna, Manjula Gururaj, Shamala Jagirdhar.

Singers
P. Kalinga Rao, Mysore Ananthaswamy, C.Aswath, Baalappa Hukkerimy, Bhimsen Joshi, Sulochana, Madikeri Nagendra, Rathnamala Prakash, Manjula Gururaj, M.K.Jayashree, H. K. Narayana, Shimoga Subbanna, Smt. Shamala Jagirdar, B. K. Sumitra, Kasturi Shankar, Raju Ananthaswamy, B.R. Chaya, Sunitha Ananthaswamy, Yashwanth Halibandi, Nagara Srinivasa Udupa, Sangeetha Katti, M.D.Pallavi, Archana Udupa, Puttur Narasimha Nayak, Rajkumar, S.Janaki, S.P.Balasubramania, Priyadarshini, Anitha Ananthaswamy, Mahesh Mahadev, Aparna Narendra, Malathi Sharma, Ameerbai Karnataki, Sangeetha Katti

Arrangers
N.S.Prasad, S.P.Venkatesh, L.Vaidyanathan, N.S.Murali, Praveen D Rao, Pravin Godkhindi, Anooru Anathakrishna Sharma, Bali

Instrumentalists
N.S.Prasad (Mandolin), Praveen Duth Stephen (Keyboard), Saadhu Kokila (Keyboard), Shabbir Ahmed (Keyboard), Krishna Udupa (Keyboard), Bali (Rhythmic Instruments), Venugopal Raju (Tabla), Praveen D Rao (Tabla and Harmonium), Srinivas Achar (Classical and 12 string Guitar), Arun Kumar (Rhythmic Instruments), Pramath Kiran (Rhythmic Instruments), N.S.Murali (Flute), Pravin Godkhindi (Flute), B.K.Chandrashekar (Violin)

Current situation and future of Sugama Sangeetha
Post Ananthaswamy and Aswath era (2000s), there are very few notable and dedicated contributors to the field. Though there were some exceptions like 'Kannadave Satya' event, Sugama Sangeetha could not get a wide base of audience. Another reason could be, the dip in standard of Kannada poetry at the same time. Even today, a full-fledged Sugama Sangeetha concert without the compositions of Kalinga Rao, Mysore Ananthaswamy and C.Aswath is hard to imagine.

Karnataka Sugama Sangeetha Pariashath's 11th annual Sugama Sangeeth conference Geethotsava – 2014 took place on 7–9 February on National College ground, Basavanagudi, Bangalore.

title: Sugama Sangeetha


text:
Talk:Translations of Gott erhalte Franz den Kaiser

The German speaking Wikipedia gives a Hebrew translation of the Kaiserhymne. The Jews of the Empire were very loyal to the monarchy, but most of them did'nt speak Hebrew. Does anybody knows about the origin or the status of this translation? --Hubertgui 00:07, 16 August 2007 (UTC)

How about English for us ignorami who don't speak any of these? Ellsworth 20:36, 2 May 2004 (UTC) Learn an little bit German, it's not difficult! --Hubertgui 00:07, 16 August 2007 (UTC)

 * Hi Ellsworth, I've really tried, but I can't find an English translation anywhere, nor is my German good enough to produce one. Native speakers, can you help?  Cheers, Opus33 21:16, 2 May 2004 (UTC)

 * I was considering putting this on the Translation into English page, but that seems to only be for articles from the other language 'pedias, not for untranslated parts of articles in this edition. Ellsworth 13:41, 3 May 2004 (UTC)

Actually, it is not a translation of Gott erhalte Franz den Kaiser but of Gott erhalte, Gott beschütze (also called Kaiserhymne, it was the Anthem of Austria between 1854 and 1918). The melody of Gott erhalte Franz den Kaiser and the Kaiserhymne is the same, but the have different lyrics. Gugganij 20:49, 21 Oct 2004 (UTC)

A Kaiserhymne (or Volkshymne) has been made for each Kaiser since Francis II/I, with the exception of Charles I., however, without an exception of Archiduke Otto. In the case of Francis and Ferdinand, even several Kaiserhymnen existed. See the German page for nearer information.

As far as I can see, the stanzas below refer to the francisco-josephinian Kaiserhymne (and not to the one of Francis II/I). A translation from the German could be the following (first stanza):
 * God save, God shelter
 * Our Kaiser, our land!
 * Mighty by means of the faith
 * He shall lead us by his wise hands!
 * Let us shelter the crown which he has inherited from his fathers
 * Against each enemy:
 * Deeply shall be united with the Throne of Habsburg
 * The future fate of Austria.

Antaios 14:45, 7 Dec 2004 (UTC)

 * Thus, the article should be moved from Translations of Gott erhalte Franz den Kaiser to for example Translations of Gott erhalte, Gott beschütze or Translation of the Kaiserhymne (1854-1918) or something similar, shouldn't it? Gugganij 11:32, 7 Dec 2004 (UTC)

I would suppose so. Possibly (especially if you look e.g. at the Italian stanza and taking into consideration that all these stanzas won't be direct translations of the German text) it would be advisable to title it "Adaptations of the Volkshymne (1854-1918) or Adaptations of the Austrian Kaiserhymne (1854-1918). Please mind that the term Kaiserhymne alone might cause confusion with the German Kaiserhymne (Heil dir im Siegerkranz). The Austrian Kaiserhymnen were also known as "Volkshymne" (People's Anthem). Antaios 14:45, 7 Dec 2004 (UTC)

Besides, the Emperor Francis is Francis II of the Holy Roman Empire (until 1806) but Francis I of Austria (as from 1804). Antaios 14:55, 7 Dec 2004 (UTC)

Copying to Wikisource
The translations should be added to the Wikisource of their respective language (or to the multl-lingual Wikisource if a Wikisource does not exist for one of the languages). --Benn Newman 22:55, 9 November 2006 (UTC)


text: User talk:68.81.71.51

title: User talk:68.81.71.51


text:
Talk:Third Punic War

Casualties
Is there a source for Carthaginian casualties? Not just for the siege of Carthage, but for the entirety of the Third Punic War? That would be a more suitable fit for this article than an unsourced number. 2601:85:C101:C9D0:B4AD:B3A5:3F74:41FD (talk) 16:20, 6 May 2021 (UTC)

conflict with another article
The article on Hasdrubal - "He was taken to Rome and displayed during Scipio's triumph, but later allowed to live in peace in Italy.[2]" - quoting Mommsen - whereas this article states his fate is/was unknown. 104.169.18.5 (talk) 10:28, 8 May 2021 (UTC)

Numidian participation.
It's pretty obvious that Numidia participated in this war. I mean the whole war started because of Numidia's attacks and the battle of Oroscopa. During the first year of the war, Numidia participated through limited combat, but by mid 148 BC a large Numidian army was sent to participate in the Siege of Carthage, and to relieve the Roman army which was harassed by Himilco Phameas's raids, after which Gulussa fought along the Roman army. In fact, the peace process itself was started after Himilco Phameas contacted Gulussa at the Roman camp to deliver his messages to the Romans. The direct participation of Numidia itself began after Scipio sent envoys into Numidia to ask for military assistance to counter Himilco's cavalry, although the first envoy had to return as Massinissa was dying. After the return of the first envoy, another was sent and were able to convince Gulussa to participate in the war by sending light cavarly commanded by himself. In fact, the captain of Carthage, Hasdrubal (not Hasdrubal the Boetharch, but another one) who was a grandson of Massinissa was executed by the Carthaginians because of his kinship ties to Gulussa, who was besieging Carthage. Whatever748 (talk) 22:22, 4 November 2022 (UTC)

 * Hi Whatever748 and thanks for bringing this up on the talk page. I am, of course, aware of most of this. As you say, the Numidians crop up several times during the war. And so are mentioned several times in the article. Do you have any specific suggestions for additions/deletions/changes to the information given about their role? (In passing, you might also like to look over Battle of Oroscopa, which I took to FA a year ago.) Gog the Mild (talk) 09:57, 5 November 2022 (UTC)
 * Hello Gog the Mild, and sorry for the late reply, i had a busy week. The article has some issues, and not just regarding the Numidians. First and foremost though, there is no mention of the core Numidian army's participation in the war (the article only mention the defection of some of the Numidian mercenary cavalry in the battle), nor Gulussa's intervention in the war, which led to the defeat of Himilco's cavalry. The article also doesn't make a distinction between Hasdrubal the Boetharch, and Hasdrubal the grandson of Massinissa (captain of Carthage, who was executed by the populace after Gulussa's arrival for his kinship ties to the Numidian kingdom). There is also no mention of the very important general Himilco Phameas, commander of the Carthaginian cavalry who was the main commander during the Battle of Lake Tunis, and of his important capitulation which happened through Gulussa's mediation. Instead, the article says that one of the Numidian commanders and his 2,200 cavalry defected to the Romans, which is false on several points, as Phameas was in no way a Numidian. While the article is well written it lacks some details and is inaccurate in some points. I'd suggest minor infobox improvements (addition of Numidia as a participant, Gulussa of Numidia in the commanders list along with Himilco Phameas), and the addition of the lacking or inaccurate details which i have mentioned above.
 * Whatever748 (talk) 19:09, 11 November 2022 (UTC)
 * My turn to apologise for my delayed response. The consensus for this article was nailed down in an unusually gruelling FAC. Which is not, of course, not to say that there is not room for improvement. You bring up a lot of points above, so I am going to pick and choose a handful to address first and we can work through the rest; possibly laying down some ground rules as we go.
 * Firstly, sources for FAs need to be high quality as well as reliable. So can I point that Smith definitely does not meet this criterion, Venning IMO doesn't (other than the introduction), Grainger is borderline - I would be loath to include something on his sole authority, Hoyos - as a professor of classics and ancient history - definitely does meet the criteria.
 * Secondly, this article is written in summary style. Just because we have a source for something is not a sufficient reason for including it. This is the reason for the exclusion of several of the issues you raise above. While this is subject to discussion, and in some cases may be a subjective judgement, the FAC consensus establishes a high bar for this being the established version.
 * Thirdly, this article is the summary of a lot of activity over several years and currently has six sub-articles. Frequently the appropriate place for detail is one of these. Or, possibly, a new sub-article - I created Battle of Oroscopa two years ago to avoid overloading this article on how and why the war started.
 * Fourthly, I am - honestly - entirely open to additions or clarifications; bearing in mind the points above.
 * To business. Which specific mention of Hasdrubal the Boetharch in this article.should actually refer to Hasdrubal the grandson of Massinissa and what is your source for each of these.
 * What is your source for "the core Numidian army's participation in the war"?
 * If you are ok with it, can we thrash out these two points before moving on to your others? Thanks. Gog the Mild (talk) 18:34, 18 November 2022 (UTC)

Regarding a revert to commas I recently added
Can we please return commas to these 6 places?

Background

“Hostages were taken and Carthage was prohibited from waging war outside Africa—and could wage war in Africa only with Rome's express permission.” (compound sentence, add comma after “taken”)

“The campaign ended in disaster at the Battle of Oroscopa and the army surrendered; many Carthaginians were subsequently massacred by the Numidians.” (Run-on/contains 3 independent clauses. Add comma after “Oroscopa” and split sentence into 2 at semicolon)

Course of the War

149 BC

“Censorinus's had the primary role of protecting the beached Roman ships and Manilius's housed the Roman legions.” (compound sentence, add comma after “ships”)

147 BC

“They had built a new fleet and once the channel was complete, the Carthaginians sailed out, taking the Romans by surprise.” (compound sentence, add comma after “fleet”)

“Fleeing Carthaginians were pursued by Rome's mounted Numidian allies and few escaped.” (compound sentence, add comma after “allies”)

Aftermath

“The Senate despatched a ten-man commission and Scipio was ordered to carry out further demolitions.” (compound sentence, add comma after “commission”) Amthisguy (talk) 16:54, 12 January 2023 (UTC)

 * Hi there. It seems to me that you are trying to insert serial commas. This article doesn't use them. I appreciate that this may make it look odd to those who are used to them, but vice versa and the MoS gives a free choice. Gog the Mild (talk) 17:31, 12 January 2023 (UTC)
 * @Gog the Mild They aren't technically serial commas, but you're still right. Can I break up the run-on though? Amthisguy (talk) 19:22, 12 January 2023 (UTC)

 * I'm unsure what/where the run on is, but feel free to go for it. If I really don't like it I can revert it and we can discuss it here. Usually I am fairly relaxed about phraseology and try not to be precious just because a form of words was the one I wrote.
 * Just as an aside, last month I had the following exchange at a FAC:
 * Reviewer: My English professors have always been insistent on comma usage, so it actually was shocking to me when I found out that not all introductory prepositional phrases needed commas!
 * Me: That sounds like my feelings when I discovered commas apparently scattered at random across an article. (My school had corporal punishment, and I would probably have received at least a smart swipe with a ruler for "Today, I ate breakfast" or "In 58 BC, Caesar invaded Gaul." Shudder! "Speech defect Gog? Pay attention!") Gog the Mild (talk) 19:48, 12 January 2023 (UTC)

Genocide characterization
This article is currently in the category "Genocides in Africa". Presumably, this characterization stems from this article which I've found from the List of genocides (where this war is listed). What should be done here? We can't have this category sitting around if its not sourced in the article—is there something more to include here?  Aza24  (talk)   03:39, 1 August 2023 (UTC)
 * Writing as the author of 87% of the article and the editor who took it through FAC, there was no genocide during the Third Punic War. Either as we understand it now nor as it was understood then. There was a protracted military operation, at the end of which the survivors of the assault on a single city were enslaved; this had happened thousands of times before and has happened thousands of times since. Then, to quote from the article: "Surviving cities were permitted to retain at least elements of their traditional system of government and culture. The Romans did not interfere in the locals' private lives and Punic culture, language and religion survived, and is known to modern scholars as "Neo-Punic civilization". The Punic language continued to be spoken in north Africa until the 7th century AD." This is all well cited to scholarly sources. Even the article "The First Genocide: Carthage, 146 BC" states "It was not a war of racial extermination. The Romans did not massacre the survivors, nor the adult males. Nor was Carthage victim of a Kulturkrieg." I consider the category entirely inappropriate, but have little energy for possible edit wars over the minutiae around every FA I write. If you have, then please feel free to remove it and watchlist the article against reinstatement. Gog the Mild (talk) 11:04, 1 August 2023 (UTC)
 * Okay, I've now removed it, as entirely unsourced. Will keep an eye on this article and have removed it from the list (we'll see if I get reverted...) –  Aza24  (talk)   20:27, 1 August 2023 (UTC)

title: Talk:Third Punic War


text:
Kathu

Kathu is a town in South Africa, and the iron ore capital of the Northern Cape province. Its name means "town under the trees", after the Camel Thorn forest it is situated in. The phrase "the town under the trees" was coined by an engineer working in the town in the early-1990s as part of a tourist marketing drive, together with the accompanying graphic. It was intended to be a marketing slogan. The meaning of the word "Kathu" has anecdotically been attributed to a porridge brewed by the local population from the powder found in the pods of the Camel Thorn trees.

Kathu was founded in the late-1960s or early-1970s.

Kathu is situated between Upington and Vryburg with about a 2-hour drive to each. Kimberley is a 3-hour drive away, while Kuruman is only 20 minutes away.

Camel thorn tree forest
The Camel Thorn tree Acacia erioloba forest is one of only two in the world with the other being between Mariental and Rehoboth in Namibia. Its unique nature was recognized in the early-1920s when it was declared a State Forest. In 1995 it was registered as a Natural Heritage Site. The Kathu Forest is approximately 4000 hectares in size and these Camel thorns trees provide support for large Sociable Weaver’s nests and are used by many other bird and animal species. In fact surveys has shown a moderate to high diversity in animal and plant species, including several Red Data, endemic and protected species in and around the forest. Bigger trees in the forest are reckoned to be older than 300 years.

Mining
The town and the accompanying industrial area of Sishen came into being because of iron ore mining activity in the Kalahari — it has one of the five largest open-cast iron ore mining operations in the world. The primary drilling and 'load and haul' mining equipment used by the mine include giant ore trucks that bear about 260 ton of ore with each load. Mining shovels used to load these trucks can weigh in excess of 800 tons and drilling equipment include drills that can drill up to 400 mm holes for blasting purposes. Some of the world's longest ore trains travel through harsh territory on the Sishen-Saldanha railway to offload their cargo at Saldanha Bay. Kumba Iron Ore is the principal mine operator in Kathu.

Recreation
Kathu has a golf course and a small, well-stocked game reserve also adjoins the town.

The town has a well established sporting complex including tennis courts, swimming pool and a golf course. One of the tennis courts is named after veteran tennis player Herta Hegewisch.

Kathu Archaeological Site Complex
Significant Stone Age sites occur in and around Kathu and on adjacent farms. These are subject to on-going archaeological research.

The importance of the Kathu Pan site was highlighted in the November 16, 2012 issue of the journal Science in which Jayne Wilkins and colleagues reveal evidence of 500 000 year-old stone points (excavated by Peter Beaumont in 1979-1982), argued to be the earliest stone-tipped spears yet found. This conclusion, based partly on study of use wear, is taken to indicate that human ancestors used stone-tipped weapons for hunting 200 000 years earlier than previously thought. Wilkins is quoted as saying that the find does more than simply extend the prehistory of stone-tipped spears – it puts those first spears firmly in the hands of Homo heidelbergensis. "Modern foragers use such tools to take down large game as part of cooperative, strategic hunts. Perhaps our ancestor did so too."

Kathu Townlands, one of the richest early prehistoric archaeological sites at Kathu, has produced tens of thousands of Earlier Stone Age artifacts, including hand axes and other tools and estimated to be between 700,000 and one million years old. It is situated between the Kuruman Hills to the east and the Langberge mountains to the west. These discovery was made in 2013 by archaeologists from the University of Cape Town and the University of Toronto, in collaboration with the McGregor Museum.

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Animal euthanasia

Animal euthanasia (euthanasia from εὐθανασία; "good death") is the act of killing an animal humanely, most commonly with injectable drugs. Reasons for euthanasia include incurable (and especially painful) conditions or diseases, lack of resources to continue supporting the animal, or laboratory test procedures. Euthanasia methods are designed to cause minimal pain and distress. Euthanasia is distinct from animal slaughter and pest control.

In domesticated animals, the discussion of animal euthanasia may be substituted with euphemisms, such as "put down" or "put to sleep" to make the wording less harsh.

Methods
The methods of euthanasia can be divided into pharmacological and physical methods. Acceptable pharmacological methods include injected drugs and gases that first depress the central nervous system and then cardiovascular activity. Acceptable physical methods must first cause rapid loss of consciousness by disrupting the central nervous system. The most common methods are discussed here, but there are other acceptable methods used in different situations.

Intravenous anesthetic
Upon administration of intravenous anesthetic, unconsciousness, respiratory then cardiac arrest follow rapidly, usually within 30 seconds.

The two-stage process that some veterinarians use includes a first shot that is a sedative to make the animal more comfortable and then a second shot that euthanizes the animal. This allows the owner the chance to say goodbye to a live pet without their emotions stressing the animal. It also greatly mitigates any tendency toward spasm and other involuntary movement which tends to increase the emotional upset that the pet's owner experiences.

For large animals, the volumes of barbiturates required are considered by some to be impractical, although this is standard practice in the United States. For horses and cattle, other drugs may be available. Some specially formulated combination products are available, such as Somulose (secobarbital/cinchocaine) and Tributame (embutramide/chloroquine/lidocaine), which cause deep unconsciousness and cardiac arrest independently with a lower volume of injection, thus making the process faster, safer, and more effective.

Occasionally, a horse injected with these mixtures may display apparent seizure activity before death. This may be due to premature cardiac arrest. However, if normal precautions (e.g., sedation with detomidine) are taken, this is rarely a problem. Anecdotal reports that long-term use of phenylbutazone increases the risk of this reaction are unverified.

After the animal has died, it is not uncommon for the body to have posthumous body jerks or a sudden bladder or bowel outburst. This is caused by the muscles of the deceased animal's body relaxing.

Inhalants
Gas anesthetics such as isoflurane and sevoflurane can be used for euthanasia of very small animals. The animals are placed in sealed chambers where high levels of anesthetic gas are introduced. Death may also be caused using carbon dioxide once unconsciousness has been achieved by inhaled anesthetic. Carbon dioxide is often used on its own for euthanasia of wild animals. There are mixed opinions on whether it causes distress when used on its own, with human experiments lending support to the evidence that it can cause distress and equivocal results in non-humans. In 2013, the American Veterinary Medical Association (AVMA) issued new guidelines for carbon dioxide induction, stating that a flow rate of 10% to 30% volume/min is optimal for the humane euthanasia of small rodents.

Carbon monoxide is often used, but some states in the US have banned its use in animal shelters: although carbon monoxide poisoning is not particularly painful, the conditions in the gas chamber are often not humane. Nitrogen has been shown to be effective, although some young animals are more resistant to the effects, and it currently is not widely used.

The use of gas chambers is not the most humane form of euthanasia as it can take up to 20 minutes to fully euthanize the animal. If the chambers are not calibrated correctly or the animal is ill, the process is only delayed further which can cause more harm to the animal.

Cervical dislocation
Cervical dislocation, or displacement (breaking or fracturing) of the neck, is an older and less common method of killing small animals such as mice. Performed properly it is intended to cause as painless a death as possible and has no cost or equipment involved. The handler must know the proper method of executing the movement which will cause the cervical displacement and without proper training and method education there is a risk of not causing death and can cause severe pain and suffering. It is unknown how long an animal remains conscious, or the level of suffering it goes through after a correct snapping of the neck, which is why it has become less common and often substituted with inhalants.

Intracardiac or intraperitoneal injection
When intravenous injection is not possible, euthanasia drugs such as pentobarbital can be injected directly into a heart chamber or body cavity. With regard to state and federal laws, one of the most humane forms of euthanizing animals is through the injection Sodium Pentobarbital. This is typically the second shot that is followed after a sedative when euthanizing animals.

While intraperitoneal injection is fully acceptable (although it may take up to 15 minutes to take effect in dogs and cats ), an intracardiac (IC) injection may only be performed on an unconscious or deeply sedated animal. Performing IC injections on a fully conscious animal in places with humane laws for animal handling is often a criminal offense.

Shooting

This can be a means of euthanasia for large animals—such as horses, cattle, and deer—if performed properly. This may be performed by means of:

 * Firearms : Traditionally used in the field for euthanizing horses, deer or other large game animals. The animal is shot in the forehead with the bullet directed down the spine through the medulla oblongata, resulting in instant death. The risks are minimal if carried out by skilled personnel in a suitable location.

 * Captive bolt gun : Commonly used by the meat packing industry to slaughter cattle and other livestock. The bolt is fired through the forehead causing massive disruption of the cerebral cortex. In cattle, this stuns the animal, though if left for a prolonged period it will die from cerebral oedema. Death should therefore be rapidly brought about by pithing or exsanguination. Horses are killed outright by the captive bolt, making pithing and exsanguination unnecessary.

Reasons
The reasons for euthanasia of pets and other animals include:
 * Terminal illness, e.g. cancer or rabies
 * Illness or accident that is not terminal but would cause suffering for the animal to live with, or when the owner cannot afford, or when the owner has a moral objection to the treatment
 * Restlessness
 * A hunter's coup de grâce
 * Behavioural problems (usually ones that cannot be corrected) e.g. aggression – Canines that have usually caused grievous bodily harm (severe injuries or death) to either humans or other animals through mauling are usually seized and euthanised ('destroyed' in British legal terms)
 * Old age and deterioration leading to loss of major bodily functions, resulting in severe impairment of the quality of life
 * Dementia in pets leading to loss of cognitive function and normal daily behaviour and interactions with owner. Dementia resulting in unsocial and repetitive behaviour causing prolonged stress for both pets and their owners.
 * Lack of home or caretaker or resources for feeding
 * Research and testing – In the course of scientific research or testing, animals may be euthanized in order to be dissected, to prevent suffering after testing, to prevent the spread of disease, or other reasons

Small animal euthanasia is typically performed in a veterinary clinic or hospital, at animal shelter, or at the pet owner's home and is usually carried out by a veterinarian or a veterinary technician working under the veterinarian's supervision. Often animal shelter workers are trained to perform euthanasia as well. Knowing when it's time to put a pet down can be difficult. A licensed veterinarian can help an owner determine when in the course of an illness or behavioral problem euthanasia is appropriate.

In the case of large animals which have sustained injuries, this will also occur at the site of the accident, for example, on a racecourse.

Some animal rights organizations support animal euthanasia in certain circumstances and practice euthanasia at shelters that they operate.

Legal status
In the U.S., for companion animals euthanized in animal shelters, most states prescribe intravenous injection as the required method. These laws date to 1990, when Georgia's Humane Euthanasia Act became the first state law to mandate this method. Before that, gas chambers and other means were commonly employed. The Georgia law was resisted by the Georgia Commissioner of Agriculture, Tommy Irvin, who was charged with enforcing the act. In March 2007, he was sued by former State Representative Chesley V. Morton, who wrote the law, and subsequently ordered by the court to enforce all provisions of the Act.

Some states allow the use of carbon monoxide chambers for euthanasia.

Remains
Many pet owners choose to have their pets cremated or buried after the pet is euthanized, and there are pet funeral homes that specialize in animal burial or cremation. Otherwise, the animal facility will often freeze the body and subsequently send it to the local landfill.

In some instances, animals euthanized at shelters or animal control agencies have been sent to meat rendering facilities  to be processed for use in cosmetics, fertilizer, gelatin, poultry feed, pharmaceuticals and pet food. It was proposed that the presence of pentobarbital in dog food may have caused dogs to become less responsive to the drug when being euthanized. However, a 2002 FDA study found no dog or cat DNA in the foods they tested, so it was theorized that the drug found in dog food came from euthanized cattle and horses. Furthermore, the level of the drug found in pet food was safe.

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Gois

Gois, De Góis or Degois can refer to:
 * Bento de Góis (1562-1607), Portuguese traveller, probably the first European to travel overland from India to China via Afghanistan
 * Damião de Góis, 16th-century Portuguese philosopher
 * Typhanie Degois (born 1992), French politician
 * The Passage du Gois, a natural, periodically flooded passage leading to the island of Noirmoutier in France
 * Góis, a town and municipality in Portugal
 * Gois (moth), a genus of moths in the family Megalopygidae

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Mark (unit)

The Mark (from Middle High German: Marc, march, brand) is originally a medieval weight or mass unit, which supplanted the pound weight as a precious metals and coinage weight in parts of Europe in the 11th century. The Mark is traditionally divided into 8 ounces or 16 lots. The Cologne mark corresponded to about 234 grams.

Like the German systems, the French poids de marc weight system considered one "Marc" equal to 8 troy ounces.

Just as the pound of 12 troy ounces (373 g) lent its name to the pound unit of currency, the mark lent its name to the mark unit of currency.

Origin of the term
The Etymological Dictionary of the German Language by Friedrich Kluge derives the word from the Proto-Germanic term marka, "weight and value unit" (originally "division, shared").

The etymological dictionary by Wolfgang Pfeifer sees the Old High German marc, "delimitation, sign", as the stem and assumes that marc originally meant "minting" (marking of a certain weight), later denoting the ingot itself and its weight, and finally a coin of a certain weight and value.

According to an 1848 trade lexicon, the term Gewichtsmark comes from the fact that "the piece of metal used for weighing was stamped with a sign or symbol". Meyer's 1905 Konversationslexikon similarly derives the origin of the word to the emergence of the mark from the Roman pound of to 11 ounces. Charlemagne, as King of the Franks, carried out a monetary and measures reform towards the end of the 8th century. In particular, he had introduced the Karlspfund ("Charles pound") as the basic unit of coinage and trade which, however, weighed only 8 ounces. In order to prevent a further reduction in the weight of a pound, a sign, the mark, was now stamped on the new weights. The actual weight of these weights, known as marca, is said to have fluctuated between 196 g and 280 g.

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Eicosanoid

Eicosanoids are signaling molecules made by the enzymatic or non-enzymatic oxidation of arachidonic acid or other polyunsaturated fatty acids (PUFAs) that are, similar to arachidonic acid, around 20 carbon units in length. Eicosanoids are a sub-category of oxylipins, i.e. oxidized fatty acids of diverse carbon units in length, and are distinguished from other oxylipins by their overwhelming importance as cell signaling molecules. Eicosanoids function in diverse physiological systems and pathological processes such as: mounting or inhibiting inflammation, allergy, fever and other immune responses; regulating the abortion of pregnancy and normal childbirth; contributing to the perception of pain; regulating cell growth; controlling blood pressure; and modulating the regional flow of blood to tissues. In performing these roles, eicosanoids most often act as autocrine signaling agents to impact their cells of origin or as paracrine signaling agents to impact cells in the proximity of their cells of origin. Some eicosanoids, such as prostaglandins, may also have endocrine roles as hormones to influence the function of distant cells.

There are multiple subfamilies of eicosanoids, including most prominently the prostaglandins, thromboxanes, leukotrienes, lipoxins, resolvins, and eoxins. For each subfamily, there is the potential to have at least 4 separate series of metabolites, two series derived from ω-6 PUFAs (arachidonic and dihomo-gamma-linolenic acids), one series derived from the ω-3 PUFA (eicosapentaenoic acid), and one series derived from the ω-9 PUFA (mead acid). This subfamily distinction is important. Mammals, including humans, are unable to convert ω-6 into ω-3 PUFA. In consequence, tissue levels of the ω-6 and ω-3 PUFAs and their corresponding eicosanoid metabolites link directly to the amount of dietary ω-6 versus ω-3 PUFAs consumed. Since certain of the ω-6 and ω-3 PUFA series of metabolites have almost diametrically opposing physiological and pathological activities, it has often been suggested that the deleterious consequences associated with the consumption of ω-6 PUFA-rich diets reflects excessive production and activities of ω-6 PUFA-derived eicosanoids, while the beneficial effects associated with the consumption of ω-3 PUFA-rich diets reflect the excessive production and activities of ω-3 PUFA-derived eicosanoids. In this view, the opposing effects of ω-6 PUFA-derived and ω-3 PUFA-derived eicosanoids on key target cells underlie the detrimental and beneficial effects of ω-6 and ω-3 PUFA-rich diets on inflammation and allergy reactions, atherosclerosis, hypertension, cancer growth, and a host of other processes.

Fatty acid sources
"Eicosanoid"  is the collective term for straight-chain PUFAs (polyunsaturated fatty acids) of 20 carbon units in length that have been metabolized or otherwise converted to oxygen-containing products. The PUFA precursors to the eicosanoids include:
 * Arachidonic acid (AA), i.e. 5Z,8Z,11Z,14Z-eicosatetraenoic acid is an ω-6 fatty acid with four double bonds in the cis configuration (denoted Z in E–Z notation), each located between carbons 5-6, 8-9, 11-12, and 14-15 (see carbon numbering).
 * Adrenic acid (AdA), i.e. 7Z,10Z,13Z,16Z-docosatetraenoic acid, is an ω-6 fatty acid with four cis double bounds, each located between carbons 7-8, 10-11, 13-14, and 16-17.
 * Eicosapentaenoic acid (EPA), i.e. 5Z,8Z,11Z,14Z,17Z-eicosapentaenoic acid is an ω-3 fatty acid with five cis double bonds, each located between carbons 5-6, 8-9, 11-12, 14-15, and 17-18.
 * Dihomo-gamma-linolenic acid (DGLA), i.e. 8Z,11Z,14Z-eicosatrienoic acid is an ω-6 fatty acid with three cis double bonds, each located between carbons 8-9, 11-12, and 14-15.
 * Mead acid, i.e. 5Z,8Z,11Z-eicosatrienoic acid, is an ω-9 fatty acid containing three cis double bonds, each located between carbons 5-6, 8-9, and 11-12.

Abbreviation
A particular eicosanoid is denoted by a four-character abbreviation, composed of:
 * its two-letter abbreviation (LT, EX or PG, as described below),
 * one A-B-C sequence-letter,
 * A subscript or plain script number following the designated eicosanoid's trivial name indicates the number of its double bonds. Examples are:
 * The EPA-derived prostanoids have three double bonds (e.g. PGG3 or PGG3) while leukotrienes derived from EPA have five double bonds (e.g. LTB5 or LTB5).
 * The AA-derived prostanoids have two double bonds (e.g. PGG2 or PGG2) while their AA-derived leukotrienes have four double bonds (e.g. LTB4 or LTB4).
 * Hydroperoxy-, hydroxyl-, and oxo-eicosanoids possess a hydroperoxy (-OOH), hydroxy (-OH), or oxygen atom (=O) substituents link to a PUFA carbon by a single (-) or double (=) bond. Their trivial names indicate the substituent as: Hp or HP for a hydroperoxy residue (e.g. 5-hydroperooxy-eicosatraenoic acid or 5-HpETE or 5-HPETE); H for a hydroxy residue (e.g. 5-hydroxy-eicosatetraenoic acid or 5-HETE); and oxo- for an oxo residue (e.g. 5-oxo-eicosatetraenioic acid or 5-oxo-ETE or 5-oxoETE). The number of their double bounds is indicated by their full and trivial names: AA-derived hydroxy metabolites have four (i.e. 'tetra' or 'T') double bonds (e.g. 5-hydroxy-eicosatetraenoic acid or 5-HETE; EPA-derived hydroxy metabolites have five ('penta' or 'P') double bonds (e.g. 5-hydroxy-eicosapentaenoic acid or 5-HEPE); and DGLA-derived hydroxy metabolites have three ('tri' or 'Tr') double bonds (e.g. 5-hydroxy-eicosatrienoic acid or 5-HETrE).

The stereochemistry of the eicosanoid products formed may differ among the pathways. For prostaglandins, this is often indicated by Greek letters (e.g. PGF2α versus PGF2β). For hydroperoxy and hydroxy eicosanoids an S or R designates the chirality of their substituents (e.g. 5S-hydroxy-eicosateteraenoic acid [also termed 5(S)-, 5S-hydroxy-, and 5(S)-hydroxy-eicosatetraenoic acid] is given the trivial names of 5S-HETE, 5(S)-HETE, 5S-HETE, or 5(S)-HETE). Since eicosanoid-forming enzymes commonly make S isomer products either with marked preference or essentially exclusively, the use of S/R designations has often been dropped (e.g. 5S-HETE is 5-HETE). Nonetheless, certain eicosanoid-forming pathways do form R isomers and their S versus R isomeric products can exhibit dramatically different biological activities. Failing to specify S/R isomers can be misleading. Here, all hydroperoxy and hydroxy substituents have the S configuration unless noted otherwise.

Classic eicosanoids
Current usage limits the term eicosanoid to: Hydroxyeicosatetraenoic acids, leukotrienes, eoxins and prostanoids are sometimes termed "classic eicosanoids"
 * ω-6 Series eicosanoids derived from arachidonic acid:
 * Hydroxyeicosatetraenoic acids (HETE) include the following metabolites of arachidonic acid:
 * 5-HETE, 12-HETE, 15-hydroxyeicosatetraenoic acid (i.e. 15-HETE), 20-hydroxyeicosatetraenoic acid (i.e. 20-HETE), and 19-HETE.
 * Leukotrienes (LT) include the following metabolites of arachidonic acid:
 * LTA4, LTB4, LTC4, LTD4, and LTE4.
 * Eoxins (EX) include the following metabolites of arachidnoic acid:
 * EXA4, EXC4, EXD4, and EXE4.
 * Prostanoids consisting of several different types:
 * Prostaglandins (PG) include the following metabolites of arachidonic acid:
 * PGG2, PGH2, PGE2, PGD2, PGF2alpha, PGA2, PGB2, (see ).
 * Prostacyclins include:
 * PGI2.
 * Thromboxanes (TX) include the following metabolites of arachidonic acid:
 * TXA2 and TXB2.
 * Cyclopentenone prostaglandins include the following metabolites of arachidonic acid:
 * PGA1, PGA2 (see Prostanoid, PGJ2, Δ12-PGJ2, and 15-deoxy-Δ12,14-PGJ2).
 * ω-6 Series eicosanoids derived from dihomo-gamma-linolenic acid. These metabolites are analogs of arachidonic acid-derived eicosanoids but lack a double bound between carbons 5 and 6 and therefore have 1 less double bound than their arachidonic acid-derived analogs. They the following:
 * PGA1, PGE1, and TXA1.
 * ω-3 Series eicosanoids:
 * Resolvins of the E series (RvE) (D series resolvins, RvD's, are metabolites of the 22-carbon ω-3 fatty acid docosahexaenoic acid; see ). RvE's include the following metabolites of eicosapentaenoic acid:
 * RvE1, 18S-RvE1, RvE2, and RvE3.
 * Other ω-3 series eicosapentaenoic acid-derived eicosanoids are analogs of ω-6 fatty acid-derived metabolites but contain a double bond between carbon 17 and 18 and therefore have one more double bound than their arachidonic acid-derived analogs. They include (HEPE is hydroxyeicosapentaenoic acid):
 * 5-HEPE, 12-HEPE, 15-HEPE, and 20-HETE; LTA5, LTB5, LTC5, LTD5, and LTE5 (see ); PGE3, PGD3, PGF3α, and Δ(17)-6-keto PGF1α; PGI3 (see ); and TXA3 and TXB3.
 * ω-9 Series eicosanoids
 * Hydroxy are derived form mead acid, is metabolized to the 3 double bond-containing analog of 5-HETE viz., 5-HETrE (see ).

Nonclassic eicosanoids
In contrast to the classic eicosanoids, several other classes of PUFA metabolites have been termed 'novel', 'eicosanoid-like' or 'nonclassic eicosanoids'. These included the following classes:
 * Oxoeicosanoids (oxo-ETE) include the following metabolites:
 * 5-Oxo-eicosatetraenoic acid (5-oxo-ETE), 12-oxo-ETE (see ), and 15-oxo-ETE, which are metabolites of arachidonic acid (see 15-Hydroxyeicosatetraenoic acid) and 5-oxo-ETrE which is a metabolite of mead acid (see ).
 * Hepoxilins (Hx) include the following arachidonic acid metabolites:
 * HxA3 and HxB3.
 * Lipoxins (Lx) include the following metabolites of arachidonic acid:
 * LxA4 and LxB4 (see Specialized pro-resolving mediators).
 * Epi-lipoxins (epi-Lx) include the following metabolites of arachidonic acid:
 * 15-epi-LxA4 (also termed AT-LxA4) and 15-epi-LxB4 (also termed AT-LxB4).
 * Epoxyeicosatrienoic acids (EET) include the following metabolites of arachidonic acid:
 * 5,6-EET, 8,9-EET, 11,12-EET, and 14,15-EET.
 * Epoxyeicosatetraenoic acids (EEQ) include the following metabolites of eicosapentaenoic acid:
 * 5,6-EEQ, 8,9-EEQ, 11,12-EEQ, 14,15-EEQ, and 15,16-EEQ.
 * Isoprostanes (isoP) are non-enzymatically formed derivatives of polyunsaturated fatty acids studied as markers of oxidative stress; they include the following arachidonic acid-derived isoP's which are named based on their structural similarities to PGs:
 * D2-isoPs, E2-isoPs, A2-isoPs, and J2-isoPs; and two epoxide-containing isoPs, 5,6-epoxyisoprostane E2 and 5,6-epoxyisoprostane A2. Some of these isoPs have been shown to possess anti-inflammatory activity (see ).
 * Isofurans are non-enzymatically formed derivatives of polyunsaturated fatty acids that possess a furan ring structure; they are studied as markers of oxidative stress. There are 256 potentially different furan ring-containing isomers that can be derived from arachidonic acid.
 * Endocannabinoids are certain glycerolipids or dopamine that are esterified to polyunsaturated fatty acids that activate cannabinoid receptors. They include the following arachidonic acid-esterified agents:
 * Arachidonoylethanolamine, 2-arachidonoylglycerol, 2-arachidonyl glyceryl ether, O-arachidonoyl-ethanolamine, and N-arachidonoyl dopamine.

Metabolism of eicosapentaenoic acid to HEPEs, leukotrienes, prostanoids, and epoxyeicosatetraenoic acids as well as the metabolism of dihomo-gamma-linolenic acid to prostanoids and mead acid to 5(S)-hydroxy-6E,8Z,11Z-eicosatrienoic acid (5-HETrE), 5-oxo-6,8,11-eicosatrienoic acid (5-oxo-ETrE), LTA3, and LTC3 involve the same enzymatic pathways that make their arachidonic acid-derived analogs.

Biosynthesis
Eicosanoids typically are not stored within cells but rather synthesized as required. They derive from the fatty acids that make up the cell membrane and nuclear membrane. These fatty acids must be released from their membrane sites and then metabolized initially to products which most often are further metabolized through various pathways to make the large array of products we recognize as bioactive eicosanoids.

Fatty acid mobilization
Eicosanoid biosynthesis begins when a cell is activated by mechanical trauma, ischemia, other physical perturbations, attack by pathogens, or stimuli made by nearby cells, tissues, or pathogens such as chemotactic factors, cytokines, growth factors, and even certain eicosanoids. The activated cells then mobilize enzymes, termed phospholipase A2's (PLA2s), capable of releasing ω-6 and ω-3 fatty acids from membrane storage. These fatty acids are bound in ester linkage to the SN2 position of membrane phospholipids; PLA2s act as esterases to release the fatty acid. There are several classes of PLA2s with type IV cytosolic PLA2s (cPLA2s) appearing to be responsible for releasing the fatty acids under many conditions of cell activation. The cPLA2s act specifically on phospholipids that contain AA, EPA or GPLA at their SN2 position. cPLA2 may also release the lysophospholipid that becomes platelet-activating factor.

Peroxidation and reactive oxygen species
Next, the free fatty acid is oxygenated along any of several pathways; see the Pathways table. The eicosanoid pathways (via lipoxygenase or COX) add molecular oxygen (O2). Although the fatty acid is symmetric, the resulting eicosanoids are chiral; the oxidations proceed with high stereoselectivity (enzymatic oxidations are considered practically stereospecific).

Four families of enzymes initiate or contribute to the initiation of the catalysis of fatty acids to eicosanoids:
 * Cyclooxygenases (COXs): COX-1 and COX-2 initiate the metabolism of arachidonic acid to prostanoids that contain two double bonds, i.e. the prostaglandins (e.g. PGE2), prostacyclins (i.e. PGI2), and thromboxanes (e.g. TXA2). The two COX enzymes likewise initiate the metabolism of: a) Eicosapentaenoic acid, which has 5 double bonds compared to the 4 double bonds of arachidonic acid, to prostanoid, prostacyclin, and thromboxane products that have three double bonds, e.g. PGE3, PGI3, and TXA3 and b) Dihomo-γ-linolenic acid, which has three double bonds, to prostanoid, prostacyclin, and thromboxane products that have only one double bond, e.g. PGE1, PGI1, and TXA1.
 * Lipoxygenases (LOXs): 5-Lipoxygenase (5-LOX or ALOX5) initiates the metabolism of arachidonic acid to 5-hydroperoxyeicosatetraenoic acid (5-HpETE) which then may be rapidly reduced to 5-hydroxyeicosatetraenoic acid (5-HETE) or further metabolized to the leukotrienes (e.g. LTB4 and LTC4); 5-HETE may be oxidized to 5-oxo-eicosatetraenoic acid (5-oxo-ETE). In similar fashions, 15-lipoxygenase (15-lipoxygenase 1, 15-LOX, 15-LOX1, or ALOX15) initiates the metabolism of arachidonic acid to 15-HpETE, 15-HETE, eoxins, 8,15-dihydroxyeicosatetraenoic acid (i.e. 8,15-DiHETE), and 15-oxo-ETE and 12-lipoxygenase (12-LOX or ALOX12) initiates the metabolism of arachidonic acid to 12-HpETE, 12-HETE, hepoxilins, and 12-oxo-ETE. These enzymes also initiate the metabolism of; a) Eicosapentaenoic acid to analogs of the arachidonic acid metabolites that contain 5 rather than four double bonds, e.g. 5-hydroxyeicosapentaenoic acid (5-HEPE), LTB5, LTC5, 5-oxo-EPE, 15-HEPE, and 12-HEPE; b) The three double bond-containing dihomo-γ-linolenic acid to products that contain 3 double bonds, e.g. 8-hydroxy-eicosatrienoic acid (8-HETrE), 12-HETrE, and 15-HETrE (this fatty acid cannot be converted to leukotrienes); and the three double bond-containing mead acid (by ALOX5) to 5-hydroperoxy-eicosatrienoic acid (5-HpETrE), 5-HETrE, and 5-oxo-HETrE. In the most studied of these pathways, ALOX5 metabolizes eicosapentaenoic acid to 5-hydroperoxyeicosapentaenoic acid (5-HpEPE), 5-HEPE, and LTB5, and 5-oxo-EPE, all of which are less active than there arachidonic acid analogs. Since eicosapentaenoic acid competes with arachidonic acid for ALOX5, production of the eicosapentaenoate metabolites leads to a reduction in the eicosatetraenoate metabolites and therefore reduction in the latter metabolites' signaling. The initial mono-hydroperoxy and mono-hydroxy products made by the aforementioned lipoxygenases have their hydroperosy and hydroxyl residues positioned in the S chiral configuration and are more properly termed 5S-HpETE, 5S-HETE, 12S-HpETE, 12S-HETE, 15S-HpETE and, 15S-HETE. ALOX12B (i.e. arachidonate 12-lipoxygenase, 12R type) forms R chirality products, i.e. 12R-HpETE and 12R-HETE. Similarly, ALOXE3 (i.e. epidermis-type lipoxygenase 3 or eLOX3) metabolizes arachidonic acid to 12R-HpETE and 12R-HETE; however these are minor products that this enzyme forms only under a limited set of conditions. ALOXE3 preferentially metabolizes arachidonic acid to hepoxilins.
 * Epoxygenases: these are cytochrome P450 enzymes which generate nonclassic eicosanoid epoxides derived from: a) Arachidonic acid viz., 5,6-epoxy-eicosatrienoic acid (5,6-EET), 8,9-EET, 11,12-EET, and 14,15-EET (see Epoxyeicosatrienoic acid); b) Eicosapentaenoic acid viz., 5,6,-epoxy-eicosatetraenoic acid (5,6-EEQ), 8,9-EEQ, 11,12-EEQ, 14,15-EEQ, and 17,18-EEQ (see Epoxyeicosatetraenoic acid); c) Dihomo-γ-linolenic acid viz., 8,9-epoxy-eicosadienoic acid (8,9-EpEDE), 11,12-EpEDE, and 14,15-EpEDE; and d) Adrenic acid viz., 7,8-epox-eicosatrienoic acid (7,8-EpETrR), 10,11-EpTrE, 13,14-EpTrE, and 16,17-EpETrE. All of these epoxides are converted, sometimes rapidly, to their dihydroxy metabolites, by various cells and tissues. For example, 5,6-EET is  converted to 5,6-dihydroxy-eicosatrienoic acid (5,6-DiHETrE), 8,9-EEQ to 8,9-dihydroxy-eicosatetraenoic acid (8,9-DiHETE, 11,12-EpEDE to 11,12-dihydroxy-eicosadienoic acid (11,12DiHEDE), and 16,17-EpETrE to 16,17-dihydroxy-eicosatrienoic acid (16,17-DiETrE
 * Cytochrome P450 microsome ω-hydroxylases: CYP4A11, CYP4A22, CYP4F2, and CYP4F3 metabolize arachidonic acid primarily to 20-hydroxyeicosatetraenoic acid (20-HETE) but also to 16-HETE, 17-HETE, 18-HETE, and 19-HETE; they also metabolize eicosapentaenoic acid primarily to 20-hydroxy-eicosapentaenoic acid (20-HEPE) but also to 19-HEPE.

Two different enzymes may act in series on a PUFA to form more complex metabolites. For example, ALOX5 acts with ALOX12 or aspirin-treated COX-2 to metabolize arachidonic acid to lipoxins and with cytochrome P450 monooxygenase(s), bacterial cytochrome P450 (in infected tissues), or aspirin-treated COX2 to metabolize eicosapentaenoic acid to the E series resolvins (RvEs) (see Specialized pro-resolving mediators). When this occurs with enzymes located in different cell types and involves the transfer of one enzyme's product to a cell which uses the second enzyme to make the final product it is referred to as transcellular metabolism or transcellular biosynthesis.

The oxidation of lipids is hazardous to cells, particularly when close to the nucleus. There are elaborate mechanisms to prevent unwanted oxidation. COX, the lipoxygenases, and the phospholipases are tightly controlled—there are at least eight proteins activated to coordinate generation of leukotrienes. Several of these exist in multiple isoforms.

Oxidation by either COX or lipoxygenase releases reactive oxygen species (ROS) and the initial products in eicosanoid generation are themselves highly reactive peroxides. LTA4 can form adducts with tissue DNA. Other reactions of lipoxygenases generate cellular damage; murine models implicate 15-lipoxygenase in the pathogenesis of atherosclerosis. The oxidation in eicosanoid generation is compartmentalized; this limits the peroxides' damage. The enzymes that are biosynthetic for eicosanoids (e.g., glutathione-S-transferases, epoxide hydrolases, and carrier proteins) belong to families whose functions are involved largely with cellular detoxification. This suggests that eicosanoid signaling might have evolved from the detoxification of ROS.

The cell must realize some benefit from generating lipid hydroperoxides close-by its nucleus. PGs and LTs may  signal or regulate DNA-transcription there; LTB4 is ligand for PPARα. (See diagram at PPAR).

Prostanoid pathways
Both COX1 and COX2 (also termed prostaglandin-endoperoxide synthase-1 (PTGS1) and PTGS2, respectively) metabolize arachidonic acid by adding molecular O2 between carbons 9 and 11 to form an endoperoxide bridge between these two carbons, adding molecular O2 to carbon 15 to yield a 15-hydroperoxy product, creating a carbon-carbon bond between carbons 8 and 12 to create a cyclopentane ring in the middle of the fatty acid, and in the process making PGG2, a product that has two fewer double bonds than arachidonic acid. The 15-hydroperoxy residue of PGG2 is then reduced to a 15-hydroxyl residue thereby forming PGH2. PGH2 is the parent prostanoid to all other prostanoids. It is metabolized by (see diagram in Prostanoid): a) The prostaglandin E synthase pathway in which any one of three isozymes, PTGES, PTGES2, or PTGES3, convert PGH2 to PGE2 (subsequent products of this pathway include PGA2 and PGB2 (see ); b) PGF synthase which converts PGH2 to PGF2α; c) Prostaglandin D2 synthase which converts PGH2 to PGD2 (subsequent products in this pathway include 15-dPGJ2 (see Cyclopentenone prostaglandin); d) Thromboxane synthase which converts PGH2 to TXA2 (subsequent products in this pathway include TXB2); and e) Prostacyclin synthase which converts PGH2 to PGI2 (subsequent products in this pathway include 6-keto-PGFα. These pathways have been shown or in some cases presumed to metabolize eicosapentaenoic acid to eicosanoid analogs of the sited products that have three rather than two double bonds and therefore contain the number 3 in place of 2 attached to their names (e.g. PGE3 instead of PGE2).

The PGE2, PGE1, and PGD2 products formed in the pathways just cited can undergo a spontaneous dehydration reaction to form PGA2, PGA1, and PGJ2, respectively; PGJ2 may then undergo a spontaneous isomerization followed by a dehydration reaction to form in series Δ12-PGJ2 and 15-deoxy-Δ12,14-PGJ2.

PGH2 has a 5-carbon ring bridged by molecular oxygen. Its derived PGS have lost this oxygen bridge and contain a single, unsaturated 5-carbon ring with the exception of thromboxane A2 which possesses a 6-member ring consisting of one oxygen and 5 carbon atoms. The 5-carbon ring of prostacyclin is conjoined to a second ring consisting of 4 carbon and one oxygen atom. And, the 5 member ring of the cyclopentenone prostaglandins possesses an unsaturated bond in a conjugated system with a carbonyl group that causes these PGs to form bonds with a diverse range of bioactive proteins (for more see the diagrams at Prostanoid).

Hydroxyeicosatetraenoate (HETE) and leukotriene (LT) pathways
The enzyme 5-lipoxygenase (5-LO or ALOX5) converts arachidonic acid into 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which may be released and rapidly reduced to 5-hydroxyeicosatetraenoic acid (5-HETE) by ubiquitous cellular glutathione-dependent peroxidases. Alternately, ALOX5 uses its LTA synthase activity to act convert 5-HPETE to leukotriene A4 (LTA4). LTA4 is then metabolized either to LTB4 by leukotriene A4 hydrolase or leukotriene C4 (LTC4) by either LTC4 synthase or microsomal glutathione S-transferase 2 (MGST2). Either of the latter two enzymes act to attach the sulfur of cysteine's thio- (i.e. SH) group in the tripeptide glutamate-cysteine-glycine to carbon 6 of LTA4 thereby forming LTC4. After release from its parent cell, the glutamate and glycine residues of LTC4 are removed step-wise by gamma-glutamyltransferase and a dipeptidase to form sequentially LTD4 and LTE4. The decision to form LTB4 versus LTC4 depends on the relative content of LTA4 hydrolase versus LTC4 synthase (or glutathione S-transferase in cells; eosinophils, mast cells, and alveolar macrophages possess relatively high levels of LTC4 synthase and accordingly form LTC4 rather than or to a far greater extent than LTB4. 5-LOX may also work in series with cytochrome P450 oxygenases or aspirin-treated COX2 to form Resolvins RvE1, RvE2, and 18S-RvE1 (see ).

The enzyme arachidonate 12-lipoxygenase (12-LO or ALOX12) metabolizes arachidonic acid to the S stereoisomer of 12-hydroperoxyeicosatetraenoic acid (12-HPETE) which is rapidly reduced by cellular peroxidases to the S stereoisomer of 12-hydroxyeicosatetraenoic acid (12-HETE) or further metabolized to hepoxilins (Hx) such as HxA3 and HxB.

The enzymes 15-lipoxygenase-1 (15-LO-1 or ALOX15) and 15-lipoxygenase-2 (15-LO-2, ALOX15B) metabolize arachidonic acid to the S stereoisomer of 15-hydroperoxyeicosatetraenoic acid (15(S)-HPETE) which is rapidly reduced by cellular peroxidases to the S stereoisomer of 15-hydroxyeicosatetraenoic acid (15(S)-HETE). The 15-lipoxygenases (particularly ALOX15) may also act in series with 5-lipoxygenase, 12-lipoxygenase, or aspirin-treated COX2 to form the lipoxins and epi-lipoxins or with P450 oxygenases or aspirin-treated COX2 to form Resolvin E3 (see ).

A subset of cytochrome P450 (CYP450) microsome-bound ω-hydroxylases metabolize arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-HETE) and 19-hydroxyeicosatetraenoic acid by an omega oxidation reaction.

Epoxyeicosanoid pathway
The human cytochrome P450 (CYP) epoxygenases, CYP1A1, CYP1A2, CYP2C8, CYP2C9, CYP2C18, CYP2C19, CYP2E1, CYP2J2, and CYP2S1 metabolize arachidonic acid to the non-classic epoxyeicosatrienoic acids (EETs) by converting one of the fatty acid's double bonds to its epoxide to form one or more of the following EETs, 14,15-ETE, 11,12-EET, 8,9-ETE, and 4,5-ETE. 14,15-EET and 11,12-EET are the major EETs produced by mammalian, including human, tissues. The same CYPs but also CYP4A1, CYP4F8, and CYP4F12 metabolize eicosapentaenoic acid to five epoxide epoxyeicosatetraenoic acids (EEQs) viz., 17,18-EEQ, 14,15-EEQ, 11,12-EEQ. 8,9-EEQ, and 5,6-EEQ.

Function, pharmacology, and clinical significance
The following table lists a sampling of the major eicosanoids that possess clinically relevant biological activity, the cellular receptors (see Cell surface receptor) that they stimulate or, where noted, antagonize to attain this activity, some of the major functions which they regulate (either promote or inhibit) in humans and mouse models, and some of their relevancies to human diseases.

Prostanoids
Many of the prostanoids are known to mediate local symptoms of inflammation: vasoconstriction or vasodilation, coagulation, pain, and fever. Inhibition of COX-1 and/or the inducible COX-2 isoforms is the hallmark of NSAIDs (non-steroidal anti-inflammatory drugs), such as aspirin. Prostanoids also activate the PPARγ members of the steroid/thyroid family of nuclear hormone receptors, and directly influence gene transcription. Prostanoids have numerous other relevancies to clinical medicine as evidence by their use, the use of their more stable pharmacological analogs, of the use of their receptor antagonists as indicated in the following chart.

Cyclopentenone prostaglandins
PGA1, PGA2, PGJ2, Δ12-PGJ2, and 15-deox-Δ12,14-PGJ2 exhibit a wide range of anti-inflammatory and inflammation-resolving actions in diverse animal models. They therefore appear to function in a manner similar to specialized pro-resolving mediators although one of their mechanisms of action, forming covalent bonds with key signaling proteins, differs from those of the specialized pro-resolving mediators.

HETEs and oxo-ETEs
As indicated in their individual Wikipedia pages, 5-hydroxyeicosatetraenoic acid (which, like 5-oxo-eicosatetraenoic acid, acts through the OXER1 receptor), 5-oxo-eicosatetraenoic acid, 12-hydroxyeicosatetraenoic acid, 15-hydroxyeicosatetraenoic acid, and 20-hydroxyeicosatetraenoic acid show numerous activities in animal and human cells as well as in animal models that are related to, for example, inflammation, allergic reactions, cancer cell growth, blood flow to tissues, and/or blood pressure. However, their function and relevancy to human physiology and pathology have not as yet been shown.

Leukotrienes
The three cysteinyl leukotrienes, LTC4, LTD4, and LTE4, are potent bronchoconstrictors, increasers of vascular permeability in postcapillary venules, and stimulators of mucus secretion that are released from the lung tissue of asthmatic subjects exposed to specific allergens. They play a pathophysiological role in diverse types of immediate hypersensitivity reactions. Drugs that block their activation of the CYSLTR1 receptor viz., montelukast, zafirlukast, and pranlukast, are used clinically as maintenance treatment for allergen-induced asthma and rhinitis; nonsteroidal anti-inflammatory drug-induced asthma and rhinitis (see aspirin-exacerbated respiratory disease); exercise- and cold-air induced asthma (see Exercise-induced bronchoconstriction); and childhood sleep apnea due to adenotonsillar hypertrophy (see ). When combined with antihistamine drug therapy, they also appear useful for treating urticarial diseases such as hives.

Lipoxins and epi-lipoxins
LxA4, LxB4, 15-epi-LxA4, and 15-epi-LXB4, like other members of the specialized pro-resolving mediators class of eicosanoids, possess anti-inflammatory and inflammation resolving activity. In a randomized controlled trial, AT-LXA4 and a comparatively stable analog of LXB4, 15R/S-methyl-LXB4, reduced the severity of eczema in a study of 60 infants and, in another study, inhaled LXA4 decreased LTC4-initiated bronchoprovocation in patients with asthma.

Eoxins
The eoxins (EXC4, EXD4, EXE5) are newly described. They stimulate vascular permeability in an ex vivo human vascular endothelial model system, and in a small study of 32 volunteers EXC4 production by eosinophils isolated from severe and aspirin-intolerant asthmatics was greater than that from healthy volunteers and mild asthmatic patients; these findings have been suggested to indicate that the eoxins have pro-inflammatory actions and therefore potentially involved in various allergic reactions. Production of eoxins by Reed-Sternburg cells has also led to suggestion that they are involve in Hodgkins disease. However, the clinical significance of eoxins has not yet been demonstrated.

Resolvin metabolites of eicosapentaenoic acid
RvE1, 18S-RvE1, RvE2, and RvE3, like other members of the specialized pro-resolving mediators) class of eicosanoids, possess anti-inflammatory and inflammation resolving activity. A synthetic analog of RvE1 is in clinical phase III testing (see Phases of clinical research) for the treatment of the inflammation-based dry eye syndrome; along with this study, other clinical trials (NCT01639846, NCT01675570, NCT00799552 and NCT02329743) using an RvE1 analogue to treat various ocular conditions are underway. RvE1 is also in clinical development studies for the treatment of neurodegenerative diseases and hearing loss.

Other metabolites of eicosapentaenoic acid
The metabolites of eicosapentaenoic acid that are analogs of their arachidonic acid-derived prostanoid, HETE, and LT counterparts include: the 3-series prostanoids (e.g. PGE3, PGD3, PGF3α, PGI3, and TXA3), the hydroxyeicosapentaenoic acids (e.g. 5-HEPE, 12-HEPE, 15-HEPE, and 20-HEPE), and the 5-series LTs (e.g. LTB5, LTC5, LTD5, and LTE5). Many of the 3-series prostanoids, the hydroxyeicosapentaenoic acids, and the 5-series LT have been shown or thought to be weaker stimulators of their target cells and tissues than their arachidonic acid-derived analogs. They are proposed to reduce the actions of their arachidonate-derived analogs by replacing their production with weaker analogs. Eicosapentaenoic acid-derived counterparts of the Eoxins have not been described.

Epoxyeicosanoids
The epoxy eicosatrienoic acids (or EETs)—and, presumably, the epoxy eicosatetraenoic acids—have vasodilating actions on heart, kidney, and other blood vessels as well as on the kidney's reabsorption of sodium and water, and act to reduce blood pressure and ischemic and other injuries to the heart, brain, and other tissues; they may also act to reduce inflammation, promote the growth and metastasis of certain tumors, promote the growth of new blood vessels, in the central nervous system, regulate the release of neuropeptide hormones, and in the peripheral nervous system inhibit or reduce pain perception.

The ω-3 and ω-6 series
The reduction in AA-derived eicosanoids and the diminished activity of the alternative products generated from ω-3 fatty acids serve as the foundation for explaining some of the beneficial effects of greater ω-3 intake. Arachidonic acid (AA; 20:4 ω-6) sits at the head of the "arachidonic acid cascade" – more than twenty eicosanoid-mediated signaling paths controlling a wide array of cellular functions, especially those regulating inflammation, immunity, and the central nervous system.

In the inflammatory response, two other groups of dietary fatty acids form cascades that parallel and compete with the arachidonic acid cascade. EPA (20:5 ω-3) provides the most important competing cascade. DGLA (20:3 ω-6) provides a third, less prominent cascade. These two parallel cascades soften the inflammatory effects of AA and its products. Low dietary intake of these less-inflammatory fatty acids, especially the ω-3s, has been linked to several inflammation-related diseases, and perhaps some mental illnesses.

The U.S. National Institutes of Health and the National Library of Medicine state that there is 'A' level evidence that increased dietary ω-3 improves outcomes in hypertriglyceridemia, secondary cardiovascular disease prevention, and hypertension. There is 'B' level evidence ('good scientific evidence') for increased dietary ω-3 in primary prevention of cardiovascular disease, rheumatoid arthritis, and protection from ciclosporin toxicity in organ transplant patients. They also note more preliminary evidence showing that dietary ω-3 can ease symptoms in several psychiatric disorders.

Besides the influence on eicosanoids, dietary polyunsaturated fats modulate immune response through three other molecular mechanisms. They (a) alter membrane composition and function, including the composition of lipid rafts; (b) change cytokine biosynthesis; and (c) directly activate gene transcription. Of these, the action on eicosanoids is the best explored.

Mechanisms of ω-3 action

In general, the eicosanoids derived from AA promote inflammation, and those from EPA and from GLA (via DGLA) are less inflammatory, or inactive, or even anti-inflammatory and pro-resolving.

The figure shows the ω-3 and -6 synthesis chains, along with the major eicosanoids from AA, EPA, and DGLA.

Dietary ω-3 and GLA counter the inflammatory effects of AA's eicosanoids in three ways, along the eicosanoid pathways:
 * Displacement—Dietary ω-3 decreases tissue concentrations of AA, so there is less to form ω-6 eicosanoids.
 * Competitive inhibition—DGLA and EPA compete with AA for access to the cyclooxygenase and lipoxygenase enzymes. So the presence of DGLA and EPA in tissues lowers the output of AA's eicosanoids.
 * Counteraction—Some DGLA and EPA derived eicosanoids counteract their AA derived counterparts.

Role in inflammation
Since antiquity, the cardinal signs of inflammation have been known as: calor (warmth), dolor (pain), tumor (swelling), and rubor (redness). The eicosanoids are involved with each of these signs.

Redness—An insect's sting will trigger the classic inflammatory response. Short acting vasoconstrictors — TXA2 — are released quickly after the injury. The site may momentarily turn pale. Then TXA2 mediates the release of the vasodilators PGE2 and LTB4. The blood vessels engorge and the injury reddens.

Swelling—LTB4 makes the blood vessels more permeable. Plasma leaks out into the connective tissues, and they swell. The process also loses pro-inflammatory cytokines.

Pain—The cytokines increase COX-2 activity. This elevates levels of PGE2, sensitizing pain neurons.

Heat—PGE2 is also a potent pyretic agent. Aspirin and NSAIDS—drugs that block the COX pathways and stop prostanoid synthesis—limit fever or the heat of localized inflammation.

History
In 1930, gynecologist Raphael Kurzrok and pharmacologist Charles Leib characterized prostaglandin as a component of semen. Between 1929 and 1932, Burr and Burr showed that restricting fat from animal's diets led to a deficiency disease, and first described the essential fatty acids. In 1935, von Euler identified prostaglandin. In 1964, Bergström and Samuelsson linked these observations when they showed that the "classical" eicosanoids were derived from arachidonic acid, which had earlier been considered to be one of the essential fatty acids. In 1971, Vane showed that aspirin and similar drugs inhibit prostaglandin synthesis. Von Euler received the Nobel Prize in medicine in 1970, which Samuelsson, Vane, and Bergström also received in 1982. E. J. Corey received it in chemistry in 1990 largely for his synthesis of prostaglandins.

title: Eicosanoid