text: Yadav 0 Report post Posted February 8, 2014 Worldwide Nepalese Students Organization (WNSO) Nepal's activities in the framework of Non-formal Human Right Education (HRE) approach among peer students at the Higher Secondary Schools and Disable School has been proved as an innovative program to promote the Human Right. The main themes of the activities were anti-discrimination and human rights education aiming to contribute to create a culture of peace and human rights for all and to enhance active participation through volunteering in schools and colleges. The program has been continued for 5 months at schools level in 2012 by the direct facilitation of Nepalese and European volunteers. The methodology of the HRE was in the framework of the non-formal education and peace education approach whereas experiential learning, cooperative learning, active participation, learning by doing were main components. Local stakeholders reported that the series HRE non formal activities strengthened the broad understanding of human rights and fundamental freedoms among students and helped to promotion of understanding, tolerance, gender equality and friendship among peers. The positive impact has observed in term of enrichment and diffusion of knowledge, skills and values of human rights issues and being aware about new aspects they were not before among the peers that increased competences to deliver HRE activities and new knowledge about human rights among students. The beneficiaries of HRE clubs have been operating the HRE clubs by their self efforts and disseminating the knowledge and skills among other peer students. Continuation from the beneficiaries after phase out and extending in grass root level is the prime factor of sustainability and replication of program- concerned experts said. Solely focusing the young people and students at education institutions to disseminate and promote the value and knowledge of Human Right is quite relevant in the present context of Nepal. It's relevancy is further high when Nepal has been facing different types of severe human rights violation at different segments of people life, for examples, freedom of expression, voices for social inclusion, women and child rights, gender based violence, civic roles and responsibilities for peace, unity, cultural of peace and respect etc. The program was implemented in collaboration with CEIPES and Youth in Action Program supported by European Commission. It is likely the first program in Nepal by its approach and volunteering model of HRE in non formal education framework at schools and college level. Related News :Across Continents in Nepal : http://wnso.org.np/news.php?newsid=35Across Continents : http://wnso.org/page/view/across-continentsAcross Continents Official Page : http://www.acrosscontinents.ceipes.org/index.phpAcross Continents News : http://wnso.org/news/view/non-formal-hre-in-higher-secondary-schools-proved-as-innovative-activity-in-nepal Quote Share this post Link to post Share on other sites


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When King George V of Hannover gave his Queen a 'castle' as a present in 1857, it was actually just a blank canvas – a hill to the south of Hannover offering panoramic views. In the same year, the royal couple began to build a summer residence, today's Marienburg Castle.
Marienburg Castle is a Gothic dream turned to reality in the 19th century by King George V, the last monarch of the Kingdom of Hannover. But how did it begin? When King George of Hannover gave his queen a 'castle' as a present in 1857, it was actually just a blank canvas – a hill to the south of Hannover offering panoramic views. In the same year, the royal couple began to build a summer residence, which Queen Marie envisioned as a romantic hilltop castle in the medieval style. Around a rectangular courtyard the Hanoverian architect Hase built a picturesque, four-winged castle that wouldn't look out of place in a book of fairytales – an awe-inspiring ensemble of craftsmanship and splendour at their very finest. The banqueting hall, which extends over two floors, remains intact to this day. It boasts an ancestral portrait gallery and a collection of splendid silver-framed furniture, crafted in 1720 by the legendary Augsburg goldsmiths. See the grandeur of a royal banquet in the dining hall with its beautifully decorated table and dinner service adorned with the Queen's coat of arms. This medieval ambience is enhanced yet further by a chapel modelled on a Parisian church and steeply vaulted galleries decorated with knights' armour. Perhaps the most magnificent room is the Queen's Library in the south-west tower. The elaborately decorated bookshelves are masterworks of German woodcarving, while the dreamlike princesses' salon has a leaded bay window and colourful paintings of fairytale scenes such as Sleeping Beauty. There is lots to see in the region around Hannover, including St. Mary's Cathedral and St. Michael's Church in Hildesheim – both of which achieved UNESCO World Heritage status in 1985 together with the treasures they contain.
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US Senator John McCain used his Twitter feed today to call Iranian President Mahmoud Ahmadinejad a "monkey." With the US government attempting diplomacy to prevent Iran from building a nuclear bomb, the former presidential nominee's tweet was ill-timed at best. It was deemed racist by some observers, including a fellow Republican congressman.
"So Ahmadinejad wants to be first Iranian in space - wasn't he just there last week?" McCain tweeted, along with the headline "Iran launches monkey into space."
McCain was comparing Iran's recent launch of a monkey into orbit with the Iranian president's stated willingness to go into space. McCain linked to a Reuters article which said the advancement of Iran's space program demonstrates Iran is "seeking to show off missile systems that have alarmed the West because the technology could potentially be used to deliver a nuclear warhead."
Accusations that McCain's joke was racist came from several directions, including from US Rep. Justin Amash (R-MI), an Arab-American lawmaker of Palestinian descent. "Maybe you should wisen up & not make racist jokes," Amash wrote to McCain on Twitter. McCain had been unmoved by criticism, tweeting simply, "Re: Iran space tweet - lighten up folks, can't everyone take a joke?"
While it's sometimes refreshing to see lawmakers use the Internet to show their true personalities, McCain's indelicate attempt at humor demonstrated why so many politicians and other prominent folks pay a public relations employee to run their Twitter feeds.
Meanwhile, Iran's nuclear program has raised concerns that Israel might invade Iran to stop it from building a bomb. US Vice President Joe Biden offered to hold bilateral talks with Iran this past weekend, a gesture that was welcomed by Iranian Foreign Minister Ali Akbar Salehi, according to Reuters. "I think it is about time both sides really get into engagement because confrontation certainly is not the way," Salehi said.


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*****Official 2012 CP Mock Draft Thread*****
First Round
1 Indianapolis Colts (Bo's Pelini) - Andrew Luck, QB, Stanford
2 St. Louis Rams (Starbucks Fan) - Justin Blackmon, WR, Oklahoma State
3 Minnesota Vikings (Marco Polo) - Matt Kalil, OT, Southern California
4 Cleveland Browns (DaKCManAP) - Robert Griffin III, QB, Baylor
5 Tampa Bay Buccaneers (Sfheic) - Morris Claiborne, CB, LSU
6 Washington Redskins (Archie Bunker) - Ryan Tannehill, QB, Texas A&M
7 Jacksonville Jaguars (Direckshun) - Melvin Ingram, DE, South Carolina
8 Miami Dolphins (BossChief) - Courtney Upshaw, OLB/DE, Alabama
9 Carolina Panthers (Dj's left nut) - Quinton Couples, DE, North Carolina
10 Buffalo Bills (htismaqe) - Whitney Mercilus, DE, Illinois
11 Kansas City Chiefs (Pestilence) - Trent Richardson, RB, Alabama
12 Seattle Seahawks (SNR) - Luke Kuechly, LB, Boston College
13 Arizona Cardinals (DeezNutz) - David DeCastro, G, Stanford
14 Dallas Cowboys (ChiefsCountry) - Dre Kirkpatrick, CB, Alabama
15 Philadelphia Eagles (doomy3) - Fletcher Cox, DT, Mississippi State
16 New York Jets (Lono) - Michael Floyd, WR, Notre Dame
17 Cincinnati Bengals (f/OAK) (Sfheic) - Janoris Jenkins, CB, North Alabama
18 San Diego Chargers (doomy3) - Riley Reiff, OT, Iowa
19 Chicago Bears (DaKCManAP) - Jonathan Martin, OT, Stanford
20 Tennessee Titans (Marco Polo) - Cordy Glenn, G, Georgia
21 Cincinnati Bengals (Sfheic) - Mark Barron, S, Alabama
22 Cleveland Browns (f/ATL) (DaKCManAP) - Nick Perry, DE/OLB, Southern California
23 Detroit Lions (Dj's left nut) - Mike Adams, OT, Ohio State
24 Pittsburgh Steelers (Archie Bunker) - Dont'a Hightower, LB, Alabama
25 Denver Broncos (DeezNutz) - Devon Still, DT, Penn State
26 Houston Texans (Lono) - Kendall Wright, WR, Baylor
27 New England Patriots (f/NO) (ChiefsCountry) - Dontari Poe, DT, Memphis
28 Green Bay Packers (SNR) - Michael Brockers, DE, LSU
29 Baltimore Ravens (Bo's Pelini) - Peter Konz, C, Wisconsin
30 San Francisco 49ers (Pestilence) - Stephen Hill, WR, Georgia Tech
31 New England Patriots (ChiefsCountry) - Mohamed Sanu, WR, Rutgers
32 New York Giants (htismaqe) - James Brown, OL, Troy
Second Round
33. Rams (Starbucks Fan) - Zach Brown, LB, North Carolina
34. Colts (Bo's Pelini) - Reuben Randle, WR, LSU
35. Vikings (Marco Polo) - Josh Robinson, CB, Central Florida
36. Buccaneers (Sfheic) - Stephen Gilmore, CB, South Carolina
37. Browns (DaKCManAP) - Alshon Jeffery, WR, South Carolina
38. Jaguars (Direckshun) - Orson Charles, TE, Georgia
39. Redskins (Archie Bunker) - Alfonzo Dennard, CB, Nebraska
40. Panthers (DJs Left Nut) - Brandon Thompson, DT, Clemson
41. Dolphins (BossChief) - Nick Foles, QB, Arizona
42. Bills (htismaqe) - Lavonte David, LB, Nebraska
43. Seahawks (SNR) - Andre Branch, DE, Clemson
44. Chiefs (Pestilence) - Kelechi Osemele, OT, Iowa State
45. Cowboys (ChiefsCountry) - Alameda Ta'amu, NT, Washington
46. Eagles (doomy3) - Brock Osweiler, QB, Arizona State
47. Jets (Lono) - Harrison Smith, S, Notre Dame
48. Patriots (ChiefsCountry) - Vinny Curry, OLB/DE, Marshall
49. Chargers (doomy3) - Coby Fleener, TE, Stanford
50. Bears (DaKCManAP) - Dwayne Allan, TE, Clemson
51. Eagles (doomy3) - Markelle Martin, S, Oklahoma State
52. Titans (Marco Polo) - Kevin Zeitler, G, Wisconsin
53. Bengals (Sfeihc) - Lamar Miller, RB, Miami (Fl.)
54. Lions (djs left nut) - Chase Minnifield, CB, Virginia
55. Falcons (BossChief) - David Wilson, RB, Virginia Tech
56. Steelers (Archie Bunker) - Amini Silatolu, G, Midwestern State
57. Broncos (Deez Nutz) - Doug Martin, RB, Boise State
58. Texans (Lono) - Josh Chapman, DT, Alabama
59. Saints (Direckshun) - Jerel Worthy, DT, Michigan State
60. Packers (SNR) - Jared Crick, DE, Nebraska
61. Ravens (Bos Pelini) - Shea McClellin, LB, Boise State
62. 49ers (Pestilence) - Jayron Hosley, CB/PR, Virginia Tech
63. Patriots (ChiefsCountry) Dwight Jones, WR, North Carolina
64. Giants (htismaqe) Ronnell Lewis, DE, Oklahoma
Third Round
65. Colts (Bos Pelini) Chris Polk, RB, Washington
66. Rams (Starbucks Fan) Ryan Miller, G, Colorado
67. Vikings (Marco Polo) Brandon Brooks, G, Miami (Ohio)
68. Browns (DaKCMan AP) Zebrie Sanders, OT, Florida State
69. Buccaneers (Stefic) Bobbie Massie, OT, Mississippi
70. Redskins (Archie Bunker) Tommy Streeter, WR, Miami (Fl)
71. Jaguars (Direckshun) Marvin McNutt, WR, Iowa
72. Dolphins (Boss Chief) Nicholas Jean-Baptiste, DT/NT, Baylor
73. Bears (DaKCMan AP) Chandler Jones, DE, Syracuse
74. Bills (htismaqe) Brian Quick, WR, Appalachain State
75. Chiefs (Pestilence) Philip Blake, OC, Baylor
76. Seahawks (SNR) - Ladarius Green, TE, Louisiana-Lafayette
77. Eagles (doomy3) - Vontaze Burfict, ILB, Arizona State
78. Chargers (doomy3) - Kendall Reyes, DT, Connecticut
79. Bears (DaKCMan AP) - Nick Toon, WR, Wisconsin
80. Cardinals (Deez Nutz) - Mitchell Schwartz, OT, California
81. Cowboys (ChiefsCountry) Brandon Weeden, QB, Oklahoma State
82. Titans (Marco Polo) Bobby Wagner, LB, Utah State
83. Bengals (Sfeihc) Ryan Broyles, WR, Oklahoma
84. Falcons (BossChief) Jack Baquette, DE Arkansas
85. Lions (DJs left nut) Trumaine Johnson, CB, Montana
86. Steelers (Archie Bunker) LaMichael James, RB, Oregon
87. Broncos (Deez Nutz) Brandon Taylor, S, LSU
88. Texans (Lono) Jamell Flemming, CB, Oklahoma
89. Saints (Direckshun) Sean Spence, LB, Miami (Fl)
90. Packers (SNR) Bruce Irvin, OLB, West Virginia
91. Ravens (Bos Pelini) Brandon Boykin, CB, Georgia
92. 49ers (Pestilence) Juron Criner, WR, Arizona
93. Patriots (ChiefsCountry) Ben Jones, C, Georgia
94. Giants (htismaqe) Bernard Pierce, RB, Temple
Fourth Round
95. Rams (Starbucks Fan) Derek Wolfe, DE/DT, Cincinnati
96. Colts (Bo's Pelini) Michael Egnew, TE, Missouri
97. Vikings (Marco Polo) Marvin Jones, WR, California
98. Eagles (doomy3) Michael Brewster, C, Ohio State
99. Browns (DaKCMan AP) Brandon Washington, G, Miami
100. Jaguars (Direckshun) Levy Adcock, OT, Oklahoma State
101. Redskins (Archie Bunker) George Iloka, S, Boise State
102. Dolphins (Boss Chief) Andrew Darko, OT, Florida State
103. Panthers (DJ's Left Nut) Brandon Mosley, OT, Auburn
104. Bills (htismaqe) Nate Potter, OT, Boise State
105. Seahawks (SNR) Kirk Cousins, QB, Michigan State
106. Chiefs (Pestlience) Jonathan Massaquoi, OLB/DE, Troy
107. Jets (lono) Cam Johnson, LB, Virginia
108. Redskins (Archie Bunker) Matt McCants, OT, UAB
109. Chargers (doomy3) Chris Givens, WR, Wake Forest
110. Bears (DaKCMan AP) Dwight Bentley, CB, Louisiana
111. Cardinals (Deez Nutz) Casey Hayward, CB, Vanderbilt
112. Cowboys (ChiefsCountry) Tank Carder, LB, TCU
113. Eagles (doomy3) Mychal Kendricks, LB, California
114. Titans (Marco Polo) Frank Alexander, DE, Oklahoma
115. Bengals (Sfeihc) Mike Martin, DT, Michigan.
116. Lions (DJ's Left Nut) Nigel Bradham, ILB, Florida State.
117. Browns (DaKCMan AP) Vick Ballard, RB, Mississippi State.
118. Steelers (Archie Bunker) Josh Norman, CB, Coastal Carolina
119. Broncos (Deez Nutz) Emmanuel Acho, OLB, Texas
120. Texans (lono) Tony Bergstrom, G, Utah
121. Saints (Direckshun) Antonio Allen, S, South Carolina
122. Packers (SNR) Quentin Saulsberry, C, Mississippi State
123. Bills (htismaqe/Nightfyre) Leonard Johnson, CB, Iowa State
124. 49ers (Pestlience) Lucas Nix, OG, Pittsburgh
125. Patriots (ChiefsCountry) Aaron Henry, S, Wisconsin
126. Giants (Nightfyre) DeQuan Menzie, DB, Alabama
Fifth Round
127. Colts (Bo's Pelini) Billy Wynn, DE/DT, Boise State
128. Broncos (Deez Nutz) Coryell Judie, CB, Texas A&M
129. Vikings (Marco Polo) AJ Jenkins, WR, Illinois
130. Browns (DaKCMan AP) Josh Kaddu, OLB, Oregon
131. Buccaneers (stefhic) Isaiah Pead, RB, Cincinnati
132. Redskins (Archie Bunker) Robert Turbin, RB, Utah State
133. Jaguars (Direckshun) Travis Lewis, LB, Oklahoma
134. Panthers (DJ's Left Nut) Greg Childs, WR, Arkansas
135. Bills (Nightfyre) Audie Cole, LB, North Carolina State
136. Dolphins (Boss Chief) T.Y. Hilton, WR, Florida International
137. Chiefs (Pestlience) Trenton Robinson, S, Michigan State
138. Bills (Nightfyre) David Molk, C, Michigan
139. Raiders (Starbuck's Fan) Ryan Steed, CB, Furman
140. Chargers (doomy3) Kyle Wilber, OLB, Wake Forest
141. Bears (DaKCMan AP) Tauren Poole, RB, Tennessee
142. Cardinals (Deez Nutz) William Vlachos, C, Alabama
143. Cowboys (ChiefsCountry) Joe Adams, WR, Arkansas
144. Eagles (doomy3) Tyrone Crawford, DE, Boise State
145. Jets (lono) Russell Wilson, QB, Wisconsin
146. Titans (Marco Polo) Garth Gerhart, C, Arizona State
147. Bengals (Sfeihc) Senio Kelemete, G, Washington
148. Falcons (Boss Chief) Shaun Prater, CB, Iowa
149. Lions (DJ's Left Nut) Adam Gettis, C, Iowa
150. Steelers (Archie Bunker) Hebron Fangupo, NT, BYU
151. Broncos (Deez Nutz) J.K. Schaffer, LB, Cincinnati
152. Texans (lono) Brandon Lindsey, LB, Pittsburgh
153. Saints (Direckshun) Demario Davis, LB, Arkansas State
154. Packers (SNR) Omar Bolden, CB, Arizona State
155. Ravens (Bo's Pelini) Jeff Allen, OL, Illinois
156. 49ers (Pestlience) Trevor Guyton, DE, California
157. Bengals (Sfeihc) Janzen Jackson, S, McNeese State
158. Giants (Nightfyre) BJ Coleman, QB, Chattanooga
Sixth Round
159. Rams (Starbuck's Fan) Ronnie Hillman, RB, San Diego State
160. Eagles (doomy3) Matt Reynolds, OT, BYU
161. Redskins (Archie Bunker) Kheeston Randall, DE, Texas
162. Buccaneers (Sfheic) James-Michael Johnson, LB, Nevada
163. Vikings (Marco Polo) Blake Gideon, S, Texas
164. Jaguars (Direckshun) Austin Davis, QB, Southern Miss
165. Cardinals (Deez Nutz) Gerell Robinson, WR, Arizona State
166. Panthers (DJ's Left Nut) Jeff Fuller, WR, Texas A&M
167. Saints (Direckshun) Winston Guy, S, Kentucky
168. Bills (Nightfyre) Ryan Lindley, QB, San Diego State
169. Seahawks (SNR) Terrance Ganaway, RB, Baylor
170. Chiefs (Pestlience) Asa Jackson, CB, Cal Poly
171. Chargers (doomy3) Cyrus Gray, RB, Texas A&M
172. Bears (DaKCMan AP) Jerry Franklin, LB, Arkansas
173. Cardinals (Deez Nutz) Jacquies Smith, LB, Missouri
174. Cowboys (ChiefsCountry) Will Blackwell, G, LSU
175. Browns (DaKCMan AP) Chris Rainey, RB, Florida
176. Broncos (Deez Nutz) Kellen Moore, QB, Boise State
177. Raiders (Starbuck's Fan) Marc Tyler, RB, USC
178. Titans (Marco Polo) Tim Benford, WR, Tennessee Tech
179. Bengals (Sfheic) Danny Trevathan, LB, Kentucky
180. Falcons (BossChief) Bryan Anger, P, California
181. Steelers (Archie Bunker) Jarius Wright, WR, Arkansas
182. Colts (Bo's Pelini) Cliff Harris, CB, Oregon
183. Texans (lono) Jack Crawford, DE, Penn State
184. Dolphins (BossChief) Delano Howell, S, Stanford
185. Packers (SNR) Markus Zusevics, OT, Iowa
186. Ravens (Bo's Pelini) Marcel Jones, OT, Nebraska
187. 49ers (Pestlience) Jerrell Young, S, South Florida
188. Eagles (doomy3) T.J. Graham, WR, North Carolina State
189. Giants (Nightfyre) Chris Owusu, WR, Stanford
Seventh Round
190. Colts (Bos Pelini) Terrell Manning, LB, North Carolina State
191. Rams (Starbucks Fan) Ben Bojicic, C, Bowling Green
192. Vikings (Marco Polo) Sean Richardson, S, Vanderbilt
193. Browns (DaKCMan AP) Tramain Thomas, S, Arkansas
194. Buccaneers (Sfheic) Donte Paige-Moss, DE, North Carolina
195. Redskins (Archie Bunker) Najee Goode, ILB, West Virginia
196. Colts (Bos Pelini) Adrien Robinson, TE, Cincinnati
197. Dolphins (BossChief) Neiko Thorpe, S, Auburn
198. Panthers (DJs Left Nut) Marcus Forston, DT, Miami (FL)
199. Bills (Nightfyre) Elvis Akpla, WR, Montana State
200. Chiefs (Pestlience) Akiem Hicks, NT, Regina
201. Lions (DJs Left Nut) Olivier Vernon, DE, Miami (FL)
202. Bears (DaKCMan AP) Jaye Howard, DT, Florida
203. Cardinals (Deez Nutz) Christian Thompson, DB, South Carolina State
204. Cowboys (ChiefsCountry) James Hanna, TE, Oklahoma
205. Vikings (Marco Polo) Tahir Whitehead, LB, Temple
206. Packers (SNR) Chandler Harnish, QB, Northern Illinois
207. Seahawks (SNR) DaJohn Harris, DT, USC
208. Chargers (doomy3) Micah Pellerin, CB, Hampton
209. Titans (Marco Polo) Jordan Bernstine, S, Iowa
210. Jaguars (Direckshun) Evan Rodriguez, TE, Temple
211. Falcons (Boss Chief) Josh Oglesby, OT, Wisconsin
212. Lions (DJs Left Nut) Josh LeRibeus, G, SMU
213. Steelers (Archie Bunker) Dominique Hamilton, DE, Missouri
214. Jets (Lono) Mike Harris, CB, Florida State
215. Texans (Lono) Justin Bethel, S, Presbyterian
216. Saints (Direckshun) Kelcie McCray, S, Arkansas State
217. Packers (SNR) Jeremy Lane, CB, Northwestern State
218. Ravens (Bos Pelini) Case Keenum, QB, Houston
219. 49ers (Pestlience) Nick Provo, TE, Syracuse
220. Chiefs (Pestlience) Blake DeChristopher, OT, Virginia Tech
221. Giants (Nightfyre) Drake Dunsmore, TE, Northwestern
222. Steelers (Archie Bunker) Aaron Corp, QB, Richmond
223. Packers (SNR) Shawn Loiseau, LB, Merrimack
224. Jets (Lono) Adonis Thomas, RB, Toledo
225. Packers (SNR) Daryl Richardson, RB, Abilene Christian
226. Jets (Lono) Matt Veldman TE, North Dakota State
227. Browns (DaKCMan AP) DeAngelo Peterson, TE, LSU
228. Steelers (Archie Bunker) Chase Ford, TE, Miami
229. Browns (DaKCMan AP) Keith Tandy, CB, West Virginia
300. Steelers (Archie Bunker) Greg Zuerlein, K, Missouri Western
301. Falcons (BossChief) Carmen Messina, LB, New Mexico
302. Chargers (doomy3) Miles Burris, LB, San Diego State
303. Bills (Nightfyre) Randy Bullock, K, Texas A&M
304. Rams (Starbucks Fan) Shaun Powell, P, Flordia State
305. Colts (Bos Pelini) Ryan Davis, LB, Bethune-Cookman
Last edited by ChiefsCountry; 04-07-2012 at 12:25 AM..
Posts: 73,525
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Lets see if Pest goes Trent Richardson or DeCastro or Martin/Rieff.
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Major sigh of relief when he slipped the extra spot. Like you, I was gonna have to go true fan because I just couldn't bring myself to reach for Michael Brockers.
Though you may go even more true-fan than me; I'd have never gone DeCastro (Martin was my guy) - but out in Seattle, the home of Marshawn Lynch and his...uh....limited explosiveness, a badass guard may be a perfect fit to blow open holes for some power football.
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4 DEs in the top 10...yikes
Richardson or OL.....?
i have no idea what pioli would do, besides trying to trade down..
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Had a legit #1 CB prospect that didn't get thrown out of school or have problems rockin' the gange fallen to me, I'd have probably still gone CB, but one Claiborne was off the board, a pass-rusher was a no-brainer for a team that finished with 31 sacks last season and couldn't so much as slow most passing games down.
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DeCastro's on my short list. Seahawk fans are bitching about John Moffitt, but he just needs a year. He'll be fine. It'd be the other guard position I consider if DeCastro's still on the board.
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unless you have a screaming need for a tackle, the value just isn't there..its why we're even considering a RB with Charles on our roster...it would be a true BPA pick..
think of a guy like Jerry Hughes, TCU, a couple of years ago...31st pick...was he that much lesser a prospect than Upshaw?
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That's just it - after the top 4 or 5, this draft just isn't stellar.
"Its more complicated than that." -- Andy Reid
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I'm not convinced that this is a bad draft for pass-rushers. Someone like Ingram really does look like he could make a Von Miller like impact.
"If there's a god, he's laughing at us.....and our football team..."
"When you look at something through rose colored glasses, all the red flags just look like flags."
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Ingram is the one that surprised me the most, imo...I watched the guy play most of the year, thought he was very good...never thought he was a top-10 pick...can't say I see the similarities to Miller at all...
but this is just chatter...
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I really really liked Ingram in this draft. He has greater upside as an OLBer than any player available this year, IMO.
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He sucks, i hope no one picks him.
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I'm using my phone and now I have a tough decision to make. Give me like an hour.
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Allright all you Pioli's out there what do you do here @ 11 with TR and DeCastro on the board? Pick one of those two or try and trade down?
IMHO, You don't pass on a guy who grades out to be an potential All-Pro. DeCastro is my pick. A while back the CHIEFS faced a similar situation with two safties they thought were good or good enough(Woods and Tounge, I believe) and they passed on Ed Reed. Oops!
You take the Ed Reed type player.
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We check over 450 stores daily and we last saw this product for £34 at House of Fraser.Go to House of Fraser
Anne Klein was an innovator; she was a passionate creator and visionary who helped define the American fashion landscape with her eponymous brand. For more than 45 years, Anne Klein has been synonymous with American style, creating clothes that are immediately recognizable for their sophistication, wear ability, and most of all, application to women s lives. Anne Klein became a brand in 1968 and changed how women thought about and bought clothes. Over the years, a succession of designers have created clothing under the Anne Klein label, including Donna Karan, who began her career under Anne s wing, Charles Nolan, Louis Dell Olio, Patrick Robinson, Isabel Toledo and Kaufman Franco. Anne Klein s legacy continues on. The world of Anne Klein has come to encompass women s wear, accessories, eyewear, watches, legwear and more. Her clothing does more than simply meet a woman s fashion needs; it provides women with a form of self-expression and confidence. Today Anne Klein reflects the original brand ethos, We make classics fashionable. Necklaces. Clean with soft dry cloth. Fashion Jewellery. Colour: metallic


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Volvo Penta TAD1351GE is an in‐line 6‐cylinder, 12.8‐liter, diesel genset engine with electronic highpressure fuel injection, overhead camshaft, turbo, and air‐cooled exhaust manifold. The TAD1351GE is a dual‐speed engine – 50 Hz/1500 rpm and 60 Hz/1800 rpm – for prime and standby power generation.
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2009 Group 4 Project
- 1 'Tropomyosin-related Kinase(Trk): a novel family of cell surface receptor tyrosine-kinase'
- 2 Mechanism of Trk Activation via multiple Signalling pathways
- 3 Current Research
- 4 Timeline
- 5 Glossary
- 6 References
- 7 2009 Group Projects
'Tropmyosin-related kinase receptors (also known as Trk or colloqiually as "Terk" receptors), are a specific family of Tyrosine kinase receptors originating from the Trk oncogene. Trk's are commonly found throughout mammalian tissue types and bear particular signifcance in embryological development and maintainence and growth of neuronal cell types. Trks appear to be a major component of a highly intricate system of receptor complexes that mediate neurotropin and growth factor control of selective cell death and differentiation. There are three particular sub-types of receptor within the Trk loci - Trk A, Trk B and Trk C - each of which is characterised by specific differences in structure and discrimation for different Neurotrophin ligands, and thus, distinct functions.
What are neurotrophins? Neurotrophins are signalling proteins (growth factors) which are expressed mostly during embryological development to regulate neuronal tissue development. There are four typical neurotropic factors – Nerve Growth Factor (NGF), Brain-derived Neurotrophic Factor (BDNF), Neurotrophin-3 (NT-3), and Neurotrophin-4 (NT-4). These factors are believed to regulate selective tissue death via the Trk receptors and the low-affinity neurotrophin receptor p75NTR. The Selectivty of NTs for various receptors is indicated in figure 1.
- Trk receptors are composed of an extracellular segment that binds polypeptide ligands, transmembrane helix, and cytoplasmic segment where the tyrosine kinase catalytic activity takes place.[1]
- TrK receptors act as dimeric transmembrane proteins. Distally, three cysteine-rich motiffs and two Leucine rich regions form a conserved NGF binding region which is common to all TrK's near the amino terminus.[1]
- Additionally, the common binding region is flanked by a pair of extracellular immunoglobulin-like domains located proximally to the cell membrane. The juxtamembrane complex contains a variable amino acid sequence suggested to determine ligand bindng affinity and specificity and may bind directly to some ligands; The localization of these peptides appears to be non-specific in tertiary NGF-TrKA complex structures however their conformation within this complex appears to indicate direct participation in complex binding.
- Further NGF binding site affinity is generated through collaboration with the p75 protein/neurotrophin receptor (p75NTR). Furthermore, p75NTR regulates NT-3-TrkA and NT-4/5-TrkB mediated receptor activation by in addition to massively increasing signal transduction sensitivity by circumnavigating the prequisite of these neurotropins for receptor activation. This is acheived through allosteric distortion of Trk binding regions.
- intracellularly, Trk shares many of the highy conserved motifs of other tyrosine kinases with some distinct variations. There are 10 conserved tyrosines in the intracellular domain, three of which, are known to contribute to the autoregulatory loop within the kinase region. Overall, 8 of the 10 tyrosines contribute to the kinase region- either by regulating kinase activity directly or by inducing adaptor protein binding including those of the Ras and phosphatidylinositol pathways. The two remaining tyrosine residues contribute to second-messenger events coupled by Shc and PLC-γ1 protein and are located outside the kinase domain.
TrK receptors achieve their function primarily via neuroptrophin signaling. There are three types of trk receptors, namely trkA, trkB and trkC. These receptors have different binding affinity to certain types of neurotrophins. Hence, the signalling by these distinct receptors will result in various cellular functions.Trk receptors regulate cell survival, proliferation, axon and dendrite growth and the expression and activity of ion channels and neurotransmitter receptors.[2] TrK also regulate synaptic strength and plasticity in adult nervous system. As a family of tyrosine kinase receptors, TrK receptors are activated and regulated in a similar fashion. TrK receptor signaling is involved in G proteins activation and pathways regulated by MAP kinase, PI3K and PLC.[3]
- Trk A
Trk A also known as Neurotrophic tyrosine kinase, receptor, type 1 is a high affinity receptor for nerve growth factor (NGF). Binding of NGF to TrK A leads to the recruitment of proteins that interact with specific phosphotyrosine residues in the cytoplasmic domains of Trk receptor A. Such interactions activate signaling pathways, such as the Ras, PI3K, and PLC pathways and result in activation of gene expression, neuronal growth and proliferation.[2][3]
- Trk B
Trk B also known as Neurotrophic tyrosine kinase, receptor, type 2 is a high affinity receptor for brain derived growth factor (BDNF) and neurotrophin-4 (NT4). Trk B are consisted of 3 isoforms in human central nervous system. The isoform (TK+) is a typical tyrosine kinase receptor, and transduce the BDNF signal via the common signaling pathways such as Ras-ERK, PI3K, and PLCγ. The other two isoforms, TKT1 and TKT2 are distinct from the typical kinase receptors as the C-terminal sequences are T1 and T2 specific.[2][3]
- Trk C
Trk C also known as Neurotrophic tyrosine kinase, receptor, type 3 is a high affinity receptor for neurotrophin-3 (NT3). Binding of NT3 on Trk C triggers the neuronal growth from neural stem cells in a process known as neurogenesis. NT3 is particularly important in proprioceptive neuron growth.[3]
Dynamic Process
NGF binding to ligation region facilitates dimerisation of Trk Receptor monomers into the signal tranductive unit- activating the kinase unit. Phosphorylation of the autoregulatory loop tyrosines of the cytoplasmic domain further activates the kinase. Phosphorylation of an additional five tyrosines within this region promotes signalling by providing docking sites for adaptor proteins which regulate signalling-cascade couples.
co-operation with p75NTR: Association with p75NTR(also known as the "low affinity neurotropin receptor") appears to be an integral component of regulation of Trk's. This combination of Trk and p75NTR proteins results in the formation of a high-affinity binding site within the Trk binding region, increasing the responsiveness of receptors for thier ligands. Additionally, coordination with p75NTR has been implicated in a reduction in ubiquitination, delay of internalisation of receptors during sensitisation, and overall decreases the apoptotic potential of cell lines.
Mechanism of Trk Activation via multiple Signalling pathways
Tropomyosine receptor kinases (Trk) enhance neuronal cell growth and differentiation of neurites via the activation of various signalling pathways. PKC, PLCy1, Ras/MAPK and PI3 are the four well known pathways, which exhibit this activity. The latter process involves the activation of transcription factors that will bind onto a specific target gene, thus trigerring neuronal cell division and/ differentiation via production of specific proteins that inhibit apoptosis.
PLC-y1 Pathway
Phospholipase C, comes in many forms and plays and important role in the signal transduction for many processes, including, proliferation, differentiation and motility. Its main function is to hydrolyze phosphatidylinositoldi phosphate (PIP2) into diacylglycerol (DAG) and inositoltriphosphate (IP3). [4] This occurs by the activation of the membrane bound receptor by a number of growth factors, cytokines and immunoglobins. [5]
DAG is necessary for the further activation of the PKC and it remains bound to the cell membrane. IP3, a water soluble protein , in turn is released into the cytoplasm and leads to the release of Ca2+ reserves from the endoplasmic reticulum. This increase of calcium ions actives the classic isoforms of [Protein Kinase C|Protein kinase C]. [6]
PKC Pathway
Protein Kinase C (PKC) is a family of nucleotide-independent, Ca2+-dependent serine kinases. [7]. At least 11 isozymes have been identified, [8] most PKC isozymes are ubiquitous and multiple members of the family can be coexpressed within the same cell leading to complex pathways. However, the basic signal transduction pathway involves the allosteric activation of PKC by the intracellular messengers diacylglycerol and Calcium ions. The inactive PKC is mainly found in the cytosol. Upon stimulation the PKC proteins translocate to the cell membrane. This translocation is the result of a cascade initiated by the binding of a number of extracellular ligands, such as, growth factors, hormones, and neurotransmitters to a G protein-coupled receptor (GPRC) found on the plasma membrane. This in turn activates a stimulating G protein which in turn activates phospholipase C (PLC). [9] A G protein is then activated, which then activates phospholipase C (PLC). The PLC cleaves phosphoinositol-4,5-bisphosphate (PIP2) into 1,2-diacylglycerol (DAG) and inositol-1.,4,5-triphosphate (IP3). [10] The IP3, couples to Ca2+ channels found on the endoplasmic reticulum releasing Ca2+ reserves. The increased concentration of calcium ions bind to inactive PKC molecules and then translocates to the plasma membrane. Here is binds to DAG giving rise to the active PKC enzyme. [7] The PKC family plays a major role in cellular signal transduction. [11]Their main roles consist in the regulation of cell proliferation, differentiation, survival and apoptosis. [12]
Ras-MAPK (mitogen-activated protein kinase) Pathway
Activation of Ras-MAPK signalling pathway is predominantly essential for promoting neuronal cell growth and differentiation. Several pathways derive from Trk receptors for activation of Ras molecules, which begin by formation of ligand-bound mitogen (BDNF or NGF) at an extracellular domain of the trk, causing receptor dimerization. This subsequently will lead to phosphorylation of the intracellular parts of the receptors, which activates Guanine Exchange factors (GEFs), such as sos, Grb2 and Shc. GEFs trigger the exchange of GDP bound to inactive Ras to GTP, resulting Ras to activate. The presence of activated Ras molecules, stimulate signaling via a major downstream pathway known as MAP kinase (mitogen-activated protein kinase)-although activated Ras, would be also capable of triggering several other downstream pathways such as PLC-y1 and PI3-kinases. (Figure..)
Mitogen-activated protein kinase (MAPK) pathway involves a series of signalling cascade. Raf is the first component of MAPK, activated by Ras-GTP on the plasma membrane. Raf then phosphorylates MEK1/2,which in turn activates the ERK1/2 by phosphorylation. ERK1/2 kinase would further phosphorylate a variety of downstream targets. These pathways may include phosphorylation of MAP 2-kinase by MAP 3-kinase on its serine and threonine amino-acid residues. Further phosphorylation of MAP- kinase by MAP 2-kinase on its serine and tyrosine amino-acid residues subsequently yields activated MAP-kinase. This results in activation of transcription factors that will lead to changes in gene expression. (Click here for well illustration of MAP-kinase pathway on You-tube) Nonetheless, aberrant Ras-MAPK signaling has been identified to be a possible factor responsible for the uncontrolled proliferation and malignancy (See "Cancer Biotherapy", current research).
PI3K (Phosphatidylinositol 3-kinase) Pathway
See also: Phosphatidylinositol 3-kinase
PI3K produces Phosphatidylinositides which promotes survival of many populations of neurons.[13] PI3K is also involved in motor neuronal diseases due to its role in tyropomyosine kinase receptors.PI3Ks have three subclasses based on their structure and substrate specificity. They are all composed of 85 kd and 110 kd subunits. The ability of PI3K to activate a number of signal proteins including some oncoproteins determines its significance in regulation of cell functions such as growth and survival, aging and malignant transformation.[13] Pl3K is also involved in the control of both malignant cell resistance to mutating agents and the sensitivity of malignant tumors to chemotherapy and radiotherapy.[14] PI3K has an array of main effectors which include the mitogen-transducing signal proteins such as protein kinase C, phosphoinositide-dependent kinases and mitogen activated protein kinases. They are activated either via their interaction with lipid products of PI3K or through PI3K-dependent phosphorylation of proteins.[15] PI3K is activated by number of growth factor receptors with intrinsic and tyrosine kinase activity. Nerve growth factor (NGF) activates PI3K in TRK to regulate cell functions.[16]
Current Research
Cancer biotherapy via targeting 'Ras / Ras-MAP-kinase' signalling pathway
Recent studies have hypothesized that receptors responsible for Ras activation would be effective target for treating human cancers (ref). Based on this hypothesis, since 1995, therapies utilizing the inhibition of Ras activation have aroused a major interest. Farnesylation is a process by which small G-proteins like Ras are activated and adhered to the cell membrane. In a recent paper (Sebti & Hamilton 2000), farnesyl transferase inhibitors were used in order to block the farnesylation of Ras proteins. The results revealed promising hopes in animal models but unfortunately have not been effective in human cancer treatment. The major downstream target of Ras-MAP-Kinase (MAPK) has also been taken as a subject for drug design. Sebolt and his colleagues showed that MAPK-inhibitors are effective in cancer therapy using mouse models (ref). It has been also suggested that Inhibition of the Ras-MAPK signaling pathway can serve as a potential therapy for NF1 in humans (ref).
Trk receptors can behave as signalling endosomes
In a recent publication, a hypothesized model was explained in which active Trk receptors are internalised into signaling endosomes during signalling transduction process (ref). The experiment that led to this understanding involved local application of NGF to axons and soma (cell bodies) of neuronal cells. It was shown that both ERK1/2 and ERK5 signaling cascades were activated. Surprisingly, application of NGF to neuronal cells at distance resulted only in activation of ERK5 pathway and NOT ERK1/2. It was then understood that activation of ERK5 in the cells somas required receptor internalisation due to inhibition by thermo-sensitive dynamin. Further investigation was conducted by local application of specific Trk-inhibitor (K252a) at either the distal axon or cell body, which blockaded the activation of ERK5 in the cell soma in the presence of NGF. Therefore, the hypothesized model in which active Trk receptors are internalised into signalling endosomes is inevitable. Nonetheless, the mechanism through which distance affects the specificity of signalling would be the future topic of investigation.
MicroRNAs are tissue specific, small non-coding RNAs, which are involved in post-trancriptional-silencing mechanism (See also: miRNA Science Overview). In non-mammals, miRNAs have been discovered to be involved in developmental process of the nervous system. For instance, in Caenorhabditis elegans, miR-273 participate in a regulatory mechanism in which ensures for the morphgenesis and differentiation of receptor neurons. Likewise, in mammalian brain tissue, recent studies show that certain miRNAs have been identified, in which suggest an important role of these small molecules in modulating Trk receptors and development of nervous system. In addition, functional regulation of these miRNAs are also linked to tumorgenesis of nervous system. For instance, three neuronal miRNAs (9,125a and 125b) are found to be involved in human neuroblastoma cell proliferation by down-modulating TrkC isoform.
under construction
- Apoptosis- Programmed cell death.
- Autophosphorylation is the term used to define the phosphorylation of a kinase protein catalysed by its own enzymatic activity.
- BDNF- Brain-derived neurotrophic growth factor is a protein that promotes activation of tropomyosine receptor kinases (trk).
- Dynamin- GTPase enzyme responsible for endocytosis in eukaryotic cells.
- ERK- Extracellular regulated kinase.
- Exons-Expressed regions of eukaryotic genes.
- Farnesyl transferase inhibitors- a class of experimental cancer drug blocks farnesylation of Ras proteins.
- GTPases are a large family of enzymes that can bind and hydrolyse guanosine triphosphate(GTP).
- Neurofibromatosis (NF)- an inherited disorder that causes production of benign tumours on nerve tissues. There are two types of NF; NF1 and NF2. NF1 is the most common disease amongst infants, also known as Recklinghausen disease.
- NGF- Nerve growth factor is a protein that promotes activation of tropomyosine receptor kinases (trk).
- Phosphorylation- A process by which a phosphate group is added to a protein that is required for its cellular activation.
- Proto-oncogene- normal cellular proteins that have the potential to cause uncontrolled cell growth when mutated.
- Oncogene- a gene that enhances uncontrolled proliferation of cells when expressed at high levels.
- Ras- small G-proteins that belong to the superfamily of monomeric GTPases. They are involved in receptor-mediated signal transduction pathways.
- ↑ 1.0 1.1 EJ, Reichardt LF. "Trk receptors: roles in neuronal signal transduction". Annu Rev Biochem. 2003;72:609-42. Retrieved 2 May 2009 from Pubmed
- ↑ 2.0 2.1 2.2 Pyle AD, Lock LF, Donovan PJ. Neurotrophins mediate human embryonic stem cell survival. Nat Biotechnology 1996;24:344–50. Retrieved 13 May 2009 from Pubmed
- ↑ 3.0 3.1 3.2 3.3 Melamed et al., A Novel Lymphocyte Singnaling Defect: trk A Mutation in the Syndrome of Congenital Insensitivity to Pain and Anhidrosis (CIPA). Journal of Clinical Immunology, 2004;24:(4)441-448. Retrieved on 13 May 2009 from Pubmed Cite error: Invalid
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- ↑ PhD, Hershel Raff. Physiology Secrets. Philadelphia: Hanley & Belfus, 2002.
- ↑ Mankidy, R., Hastings, J., & Thackeray, J. (2003). Distinct Phospholipase C-#-Dependent Signaling Pathways in the Drosophila Eye and Wing Are Revealed by a New small wing Allele. Genetics Society of America. 164(2): 553–563.
- ↑ Bioengineering; Research from University of Tokyo broadens understanding of bioengineering. (2009,May). Medical Devices & Surgical Technology Week,70.
- ↑ 7.0 7.1 Takai, Y., Kishimoto, A., Inoue, M., & Nishizuka, Y. (1977). Studies on a cyclic nucleotide-independent protein kinase and its proenzyme in mammalian tissues. I. Purification and characterization of an active enzyme from bovine cerebellum. J. Biol. Chem., 252(21), 7603-7609. [1]
- ↑ Acs, P., Wang, Q., Bogi, K., Marquez, A., Lorenzo, P., Biro, T., Szallai, Z., Mushinski, F., & Blue, P. (1997). Both the Catalytic and Regulatory Domains of Protein Kinase C Chimeras Modulate the Proliferative Properties of NIH 3T3 Cells. J Biol Chem., 272(45), 28793-28799. Retrieved May 15, 2009, from Pubmed
- ↑ Dekker, L (2004). Protein Kinase C (Molecular Biology Intelligence Unit). New York: Springer.
- ↑ Signal Transduction Resource. (n.d.). Retrieved May 15, 2009, from Promega
- ↑ Steinberg, S. (2008). Structural Basis of Protein Kinase C Isoform Function. Physiol. Rev., 88, 1341-1378. Retrieved October 5, 2009, from Pubmed
- ↑ D Breitkreutz, L Braiman-Wiksman, N Daum, M F Denning, T Tennenbaum. (2007). Protein kinase C family: On the crossroads of cell signaling in skin and tumor epithelium. Journal of Cancer Research & Clinical Oncology, 133(11), 793-808. Retrieved May 16, 2009, from Pubmed
- ↑ 13.0 13.1 Krasilnikov MA. Phoshatidylinositol-3 kinase dependent pathways: the role in control of cell growth, survival, and malignant transformation. Biochemistry. Review 2000;65(1):59-67. Retrieved May 16, 2009, from Pubmed Cite error: Invalid
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- ↑ Carpenter et al., A tightly associated serine/threonine protein kinase regulates phosphoinositide 3-kinase activity. Molecular Cell Biology. 1993;13(3):1657-1665. Retrieved May 16, 2009, from Pubmed
- ↑ Kapeller R, and Cantley LC. Phosphatidylinositol 3-kinase. Bioessays. 1994;16(8):565-576. Retrieved May 16, 2009, from [2]
- ↑ Stephens LR, Jackson TR, and Hawkins PT. Agonist-stimulated synthesis of phosphatidylinosital(3,4,5)-triphosphate: a new intracellular signaling system? Biochim Biophys Acta 1993;1179(1):27-75. Retrieved May 16, 2009, from Pubmed
- Ardem Patapoutian, and Louis F. Reichardt. "Trk receptors: mediators of neurotrophin action"Current Opinion in Neurobiology. Volume 11, Issue 3, 1 June 2001, Pages 272-280
- J. and Ashford, M.L.J. "Leptin in the CNS: much more than a satiety signal". Neuropharmacology. 2003;44, 845-854.
- Sebti S.M., Hamilton A.D,. "Farnesyltransferase and geranylgeranyltransferase I inhibitors and cancer therapy: lessons from mechanism and bench-to-bedside translational studies". Oncogene.(2000).19(56): 6584-93.
- J.S,. Dudley D.T,. Herrera.R, Van Becelaere.K, Wiland A, Gowan RC, Tecle H, Barrett SD, Bridges A, Przybranowski.S,. Leopold WR. Saltiel A.R,. "Blockade of the MAP kinase pathway suppresses growth of colon tumors in vivo". Nat Med. (1999).5(7): 810-6.
- N.E., Omer C.A., Conner MW., Anthony NJ, Davide JP, deSolms SJ, Giuliani EA, Gomez RP., Graham SL., Hamilton K., "Inhibition of farnesyltransferase induces regression of mammary and salivary carcinomas in ras transgenic mice". Nat Med (1995).1(8): 792-7.
- FL, Heerssen HM, Bhattacharyya A, Klesse L, Lin MZ, Segal RA."Neurotrophins use the Erk5 pathway to mediate a retrograde survival response".Nat Neurosci.2001;4(10):981-8
- DR, Wu YM, Lin SF. The protein tyrosine kinase family of the human genome. Oncogene. 2000;19(49):5548-57.
- G, Whyte DB, Martinez R, Hunter T, Sudarsanam S. The protein kinase complement of the human genome. Science. 2002;298(5600):1912-34.
- EJ, Reichardt LF. Trk receptors: roles in neuronal signal transduction. Annu Rev Biochem. 2003;72:609-42.
- Miska EA, Alvarez-Saavedra E, Townsend M, Yoshii A, Sestan N, Rakic P, Constantine-Paton M, Horvitz HR. "Microarray analysis of microRNA expression in the developing mammalian brain". Genome Biol. 2004;5(9):R68
- Smirnova L, Gräfe A, Seiler A, Schumacher S, Nitsch R, Wulczyn FG. "Regulation of miRNA expression during neural cell specification". Eur J Neurosci. 2005;21(6):1469-77
2009 Group Projects
--Mark Hill 14:02, 19 March 2009 (EST) Please leave these links to all group projects at the bottom of your project page.
Group 1 Meiosis | Group 2 Cell Death - Apoptosis | Group 3 Cell Division | Group 4 Trk Receptors | Group 5 The Cell Cycle | Group 6 Golgi Apparatus | Group 7 Mitochondria | Group 8 Cell Death - Necrosis | Group 9 Nucleus | Group 10 Cell Shape


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With April here, and following a rather good first quarter for equities (see below) it's that time of the year to once again debunk one of the great myths of investing.
Each May, throngs of investors sell their stocks, only to buy them again in early November. The so-called "sell in May and go away" crowd believe that the seasonal tendency of equities to swoon in the summer months and into early fall is so persistent that it makes sense to only own stocks for the six months beginning in November.
Recent results have made more believers. Consider last year's drawdown in stocks brought about by fears of a European economic collapse. A good chunk of the pain from 2008 could have been avoided from that year's meltdown as well.
Is there anything to this strategy? A number of academic papers have shown that there is a tendency for stocks to underperform in the middle of the year. One study showed that the effect holds true in 36 of 37 developed and emerging markets studied. Even so, here are three reasons to think twice before dumping stocks next month and re-buying after Halloween:
Reason 1: Data Mining
In reality, market returns are so volatile that taking away or adding just a few days from each summer period typically eliminates any seasonal effect. And since most May-October periods end with smaller but still meaningful profits than the other six months of the year, investors are missing out on gains they would have achieved from a buy-and-hold strategy. It isn't as though the equity risk premium suddenly disappears when the weather gets warm.
Reason 2: Taxes
Those choosing to own stocks six months out of the year pay a 35% short-term capital gains rate, while those that buy and hold pay a 15% long-term capital gains rate. Sadly, the seasonal "tendency" of stocks to underperform during the May-October period isn't likely to make up that gap over the long haul.
Reason 3: Dividends
Dividends are the economic rent investors are paid for holding equity securities. Historically, they make up a good chunk of the total return from buy-and-holders. Obviously, one would cut their income in half following the Sell in May mantra.
Like many thematic strategies, selling in May is an interesting data artifact. But for serious investors, it's just another pothole to avoid on the long road to success.


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Among some of the stereotypes perpetuated about young investors are that they rely on social media for financial guidance, ignore professional advice and resist proven methods for investing. However, a survey released Tuesday by Merrill Lynch Private Banking and Investment Group found those stereotypes may be largely exaggerated.
The Young High-Net-Worth Insights Survey was conducted in February by Phoenix Marketing International among 153 investors between 18 and 35 who had at least $1 million in investable assets.
Most respondents said they understood their parents' approach to investing and of those, many say their own investing style was similar. More than two-thirds said their parents had the right idea about investing and 65% said their parents' approach still worked in today's economy. Less than half said they knew more about finance or investing than their parents.
"Young investors want to know what to do over time and how to align that with their goals," Michael Liersch, director of behavioral finance for Merrill Lynch, told AdvisorOne on Monday. They want to understand their investments and strategy, but they want guidance, too. Just 19% of young investors said they had a high level of understanding of financial subjects, and 25% said they had very little knowledge.
Almost 60% of respondents said they work with an advisor, but 72% of those also think of themselves as self-directed investors. "A lot of investors have the notion that you're either conservative or aggressive; you're self-directed or work with an advisor," Liersch said. "You can be all of the above."
In looking for an advisor, someone who understands their needs is the most important criterion, the survey found. "They want to be seen as a unique individual," Liersch said, "and how they want that done is most critical. Start with the idea that there are no right or wrong decisions. There's just the right approach for you."
The majority of young investors are trying to grow their assets, while 12% are trying to preserve them. Nearly two-thirds said they would take on more risk for better returns. To reduce risk, 78% of young investors said they would make diversification a priority.
No matter how many times young investors log on to update their status or retweet a post, they still rely primarily on traditional media for financial information. Nearly 60% said they watch business news programs on television, 55% said they read newspapers and 52% said they read magazines for financial news. Just 27% said they use social media or blogs for their financial information.
"Social media is not helping young investors formulate their financial strategy," Liersch said. "They want human interaction to do that." Liersch stressed that social media is just one part of advisors' approach to marketing to and communication with younger investors.
Frank Migliazzo, a private wealth advisor for Merrill Lynch agreed with that assessment, adding that in his practice he uses face-to-face meetings, email, research blasts and video conferencing as part of his overall marketing and communication strategy.
The survey found that some young investors in wealthy don't talk about finances with their parents out of fear of disappointing their families or appearing entitled. Just 46% of respondents said they talk about financial matters with their parents.
"Regardless of inheritance, different families come with different philosophies about money," Liersch said. He suggested there are two categories for how families approach money and finances with their kids. Some families communicate as much as possible, he said, while others avoid it because they don't want money to define who they are as a family. "Both come from a positive place," he said.


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SIM unlock code of all Sony is available, means Sony Xperia XA1 Ultra can be unlocked easily with unlock code. It is fast and secure way to unlock Sony phone by IMEI. You can unlock all Sony Xperia XA1 Ultra devices from any network. Once the restriction is removed, you can use all GSM simcards on your phone.
To unlock your phone, we need only 15-digits IMEI. You can find the 15-digit correct IMEI by dialing *#06# on the phone.
Unlocking of the Sony Xperia XA1 Ultra by code does not avoid warranty. It is recommended method by manufacturer of Sony to unlock the phone by code.
The unlock code of Sony Xperia XA1 Ultra comes from the database of manufacturer or network provider, means it will work 100%.


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Vietnam visa for citizens of Northern Ireland
Do Irish passport holders need a visa to Vietnam?
Yes, Northern Ireland passport holders need a visa to Visit Vietnam.
How to apply Vietnam visa for citizens of Northern Ireland?
There are two options:
Option 1: Obtain the letter of approval to pick up the visa upon arrival at Vietnam airport (get visa stamped at Vietnam International Airports on arrival).
Visa on arrival is beneficial for those who live far away from the Vietnamese embassies and do not wish to send their passports away by postal mail.
– Issuing unit: Vietnam Immigration Department
– Processing time: 1 to 2 working days
– No Passport sendoff required
– How it works? You go online at https://www.visainvietnam.org/booking, fill in the secure form, and just wait 2 working days (normal service) or within 1 working day (urgent service) to get your Visa Approval Letter via email, and take this letter + your passport + 2 photos + pay a stamping fee of $45 for single entry and $ 65-95 for multiple entries. Make sure that you bring the cash with you because you might not find any ATMs near you.
Don't forget to check the approval letter to make sure that all the information is correct. If you find any processing mistakes, we'll refund the charges and make you a new one.
Option 2: Contact the Embassy of Vietnam in Northern Ireland before you arrive Vietnam. The procedures are quick and simple.
– Issuing unit: Vietnam Embassy
– Processing time: 4 to 5 working days
– Your original passport required
– Before applying for Vietnam visa, make sure your passport has minimum 6 month validity and left pages.
– For visa on arrival option, it is applicable for those traveling by air to Vietnam.
– If you travel on a cruiseship, please contact the cruise operator for visa procedures.


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Acpitool: commandline ACPI status program for laptops
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Joined: 20 Jan 2006
Posts: 6759
Location: hobart
Posted: Thu 24 Jul 2008, 08:31
Post subject:
Acpitool: commandline ACPI status program for laptops
AcpiTool is (yet another) Linux ACPI client. It's a small command-line application, intended to be a replacement for the apm tool. The primary target audience are laptop users, since these people are most interested in stuff like battery status, thermal status and the ability to put their precious laptop to sleep. Most of this does not apply to desktop systems.
Besides "basic" ACPI information like battery status, AC presence, etc . . . , Acpitool also supports various extensions for Toshiba, Asus and IBM Thinkpad laptops, allowing you to change the LCD brightness level, toggle fan on/off, and more.
The program simply accesses the /proc/acpi or /sysfs entries to get/set acpi values. Hence, you need a computer running a Linux kernel from the 2.4.x or 2.6.x series with acpi enabled, to use this program.
# acpitool --help
Usage: acpitool [option] . . .
Shows ACPI information from the /proc/acpi filesystem, like battery status,
temperature, or ac power. Can also suspend your machine (if supported).
-a, --ac_adapter AC adapter information
-A, --Asus show supported Asus ACPI extensions (LCD brightness level, video out routing DSTD/acpi4asus info)
-b battery status, available batteries only
-c, --cpu CPU information (type, speed, cache size, frequency scaling, c-states, . . .)
-B, --battery battery status, all info on all battery entries
-e show just about everything
-f, --fan show fan status
-F x force fan on (x=1) or switch back to auto mode (x=0). (Toshiba only)
-h, --help show this help screen
-j eject ultrabay device (Thinkpad only)
-l x set LCD brightness level to x, where x is 0..7 (Toshiba and Thinkpad only)
-m x switch the mail led on (x=1) or off (x=0) (Asus only)
-n x switch the wireless led on (x=1) or off (x=0). (Asus only)
-o x set LCD on (x=1) or off (x=0). (Asus only)
-s, --suspend suspend to memory (sleep state S3), if supported
-S suspend to disk (sleep state S4), if supported
-t, --thermal thermal information, including trip_points
-T, --Toshiba show supported Toshiba ACPI extensions (LCD brightness level, video out routing, fan status)
-v be more verbose (more detailed error messages, only usefull combined with other options)
-V, --version show application version number and release date
-w, --wakeup show wakeup capable devices
-W x enable/disable wakeup capable device x. The x can be seen when invoking -w first.
-z x set Asus LCD brightness level to x, where x is 0..15 (Asus only).
If invoked without options, acpitool displays information about available batteries,
AC adapter and thermal information.
For more info, type man acpitool at the prompt.
AcpiTool v0.5, released 24-Jul-2008
Homepage: http://freeunix.dyndns.org:8000/site2/acpitool.shtml
8745 Time(s)
Last edited by muggins on Tue 18 Aug 2009, 20:23; edited 1 time in total
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Joined: 31 May 2008
Posts: 3217
Posted: Sat 26 Jul 2008, 06:38
Post subject:
Thanks for the tool; now my Dell Latitude suspends correctly. I wasn't able to suspend via the keyboard with a USB mouse. (pointer would disappear...also couldn't restart x)
I noticed that when using ACPI, the CPU runs at max most of the time. When I boot without it, the CPU runs at min most of the time. (I'll run a few times and post the stats.)
997500 80419
731500 18609
total_trans= 957
current frequency: 997500
997500 1586
731500 11713
total_trans= 21
current frequency: 731500
Edit: I guess the CPU just has more to do with ACPI on. After an hour or so, it's doing much better...using minumum CPU state over 1.5 X max; also doing a good job cooling.
Edit2: After a day just sitting there (not using), with ACPI on it's using max CPU almost 4X as much as min; seems like a real waste of energy compared with APM.
997500 3834850
731500 998955
total_trans= 39415
current frequency: 997500
Last edited by jpeps on Sun 27 Jul 2008, 01:51; edited 1 time in total
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Joined: 15 Oct 2007
Posts: 1698
Location: Germany
Posted: Sat 26 Jul 2008, 18:55
Post subject:
hi muggins,
yes it's great
acpitool -s
works for me (too), it's brilliant.
with this and the scaling-governor-tips from
it's getting better every day.
now i had to set up my fn-keys with xbindkeys and ... my laptops will be setup'ed quite nice.
p.s. ok, after that i had to discover how temp and fan-readout works with my lenovo, but this is a new chapter as i don't need this...
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Joined: 08 Jul 2007
Posts: 739
Posted: Fri 15 Aug 2008, 07:36
Post subject:
i just tried to run acpitool -s on my desktop computer
it really turned off
but when i pushed the button i got the desktop i left in just 3 seconds
what is really happening?
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Joined: 20 Jan 2006
Posts: 6759
Location: hobart
Posted: Fri 15 Aug 2008, 23:40
Post subject:
Hello Magerlab,
option is for suspend/sleep, which I imagine must be like standby.
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Joined: 25 May 2008
Posts: 28
Location: Germany
Posted: Sat 16 Aug 2008, 21:38
Post subject:
I also installed acpitool on my toshiba laptop, but it is a very old toshiba laptop.
I'd like to know if in the livecd of puppy4, is the vmlinuz-kernel generally acpi-enabled or not because I booted with "acpi=force" and acpitool says I have no acpi-extensions installed, not even Toshiba.
Does a tool exist that allows to enable acpi on laptops that may have a bios bug, being the reason why acpi is not detected by puppy?
:Wer nicht wa:hlt, hat nichts zu melden/maulen.
:Those not voting have nothing to say/moan about.
Puppy 4.21; CD2HDD; AMD64 & X86. Slow: Laptop x86-PI@133MHz-64mb RAM (modded Puppy); Fast:Laptop email@example.com RAM.
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Joined: 20 Jan 2006
Posts: 6759
Location: hobart
Posted: Sat 16 Aug 2008, 23:24
Post subject:
Hi Monson,
what about do get from entering the following?
ls /proc/acpi
ls /proc/acpi/toshiba
Also what model toshiba do you have? Do you know what sort of BIOS it has? Toshiba? Phoenix?
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Joined: 27 Jun 2005
Posts: 443
Location: VT USA
Posted: Sun 24 Aug 2008, 12:35
Post subject:
This is a wonderful tool! Thank you so much. I think with a bit more research thyis is just what I have been looking for.
Interesting, on my T30 Thinkpad the -s suspends the lcd but not the backlight, of course that is done with the lid button but it is really interesting to see the strange patterns when the power is removed from the controller.
I will look into the sensors for these buttons and see if I can get it to work automatically.
I have not had a PupTop that suspended correctly since apm on the old 600e Thinkpads. This is a major step forward in Mobile Puppy. I am running 4.0 full hd.
Edit: I created a script to run the command and a hotkey F4 and that is good. The laptop wakes with the Fn key or when the lid is opened but there is a catch of the backlight staying on. After suspending, the cover switch does ot shut the backlight off.
Still searching but really hopeful
terminal in proc/acpi reports the following when the lid switch is pressed and released.
# cat event
ibm/hotkey HKEY 00000080 00005001
ibm/hotkey HKEY 00000080 00005002
Fn+F4 reports
ibm/hotkey HKEY 00000080 00001004
Who knows how to translate this information into commands?
If I could use the 5001 which shuts the backlight off and sleep2 then the acpitool -s it would be perfect.
Puppy Linux...
It just works!
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Joined: 21 Nov 2006
Posts: 2
Location: Germany
Posted: Tue 16 Sep 2008, 05:41
Post subject:
I've tried it on my Asus eeepc 701. the sleep command acpitool -s works. but the only way to wake it up is with tne powerbutton and the worst is after waking up the display is still dark. Maybe the backlight is off.
does somebody know how to fix it?
regards Joeboy
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Joined: 27 Sep 2007
Posts: 160
Location: A house with broken Windows
Posted: Mon 29 Sep 2008, 12:00
Post subject:
Might want to check this out:
One problem that is not listed here: on my eee 701, I find my wireless dead after a resume. A scan reveals that no access points are available regardless of how many times I toggle the wireless card on and off. Anyone else with this problem?
I've tried it on my Asus eeepc 701. the sleep command acpitool -s works. but the only way to wake it up is with tne powerbutton
Just for the record, the default xandros OS does this as well, so I think it is a hardware thing rather than something wrong with this. I actually like that it does this.
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Joined: 27 Jun 2005
Posts: 443
Location: VT USA
Posted: Tue 30 Sep 2008, 21:53
Post subject:
I had not installed the acpitool on my newest laptop with 3.01 and when I ran the suggested test from the thinkwiki
# echo mem > /sys/power/state
It suspended fine. I forgot that you need to use the Fn key to wake it up so I was a bit nervous for a minute. It still does not shut off the backlight. I have found there is an app called radeontool which does that. I will see if I can get that working next.
Puppy Linux...
It just works!
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Joined: 27 Jun 2005
Posts: 443
Location: VT USA
Posted: Wed 01 Oct 2008, 00:15
Post subject:
Ok I a stuck again. Tere seeme to be very little doccumentation for radeontool.
I was able to find a .deb and undeb it but it reports.
# radeontool
Radeon hardware not found in lspci output.
I checked with the 3DCC and it reports.
Your /var/log/Xorg.0.log reports you have this card:
(--) PCI:*(1:0:0) ATI Technologies Inc Radeon Mobility M7 LW [Radeon Mobility 7500] rev 0, Mem @ 0xe0000000/27, 0xc0100000/16, I/O @ 0x3000/8
lspci reports
00:00.0 Class 0600: 8086:1a30 (rev 04)
00:01.0 Class 0604: 8086:1a31 (rev 04)
00:1d.0 Class 0c03: 8086:2482 (rev 02)
00:1d.1 Class 0c03: 8086:2484 (rev 02)
00:1d.2 Class 0c03: 8086:2487 (rev 02)
00:1e.0 Class 0604: 8086:2448 (rev 42)
00:1f.0 Class 0601: 8086:248c (rev 02)
00:1f.1 Class 0101: 8086:248a (rev 02)
00:1f.3 Class 0c05: 8086:2483 (rev 02)
00:1f.5 Class 0401: 8086:2485 (rev 02)
00:1f.6 Class 0703: 8086:2486 (rev 02)
01:00.0 Class 0300: 1002:4c57
02:00.0 Class 0607: 104c:ac55 (rev 01)
02:00.1 Class 0607: 104c:ac55 (rev 01)
02:02.0 Class 0607: 104c:ac50 (rev 01)
02:08.0 Class 0200: 8086:1031 (rev 42)
03:00.0 Class 0c03: 1033:0035 (rev 43)
03:00.1 Class 0c03: 1033:0035 (rev 43)
03:00.2 Class 0c03: 1033:00e0 (rev 04)
I have read that you can rename the device radeon but I have no idea how to do that.
hardinfo reports a pci device
Class 0607 : 104c:ac55
the vendor id,
oem vendor 1014:0517
bus, device, function 1,0,0
relates to the correct video adapter Radeon 7500 128mb prefetchable, etc.
Perhaps something is being improperly detected. Is there another tool that could give me more information or do I already have more than enough?[/code]
Puppy Linux...
It just works!
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Joined: 26 Mar 2009
Posts: 20
Posted: Sat 04 Apr 2009, 13:25
Post subject:
I've installed acpitool on my Toshiba Tecra 8100 in an attempt to troubleshoot a non running fan.
None of the fan or temperature commands seem to work, and when I try the -T command I get:
Sorry, but no Toshiba ACPI extensions were found on this system.
Edit after remembering how to copy/paste
# acpitool -e
Kernel version : 184.108.40.206 - ACPI version : 20070126
Battery status : <not available>
AC adapter : <info not available or off-line>
Fan : <not available>
CPU type : Pentium III (Coppermine)
CPU speed : 697.433 MHz
Cache size : 256 KB
Bogomips : 1395.89
Function Show_CPU_Info : could not read directory /proc/acpi/processor/
Make sure your kernel has ACPI processor support enabled.
Thermal info : <not available>
wakeup devices : <not available>
Any thoughts?
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Joined: 20 Jan 2006
Posts: 6759
Location: hobart
Posted: Sat 04 Apr 2009, 16:07
Post subject:
if you run
does it show the toshiba_acpi module as being loaded? If not, try adding it to the Bootmanager list of modules to load, reboot, and see whether that makes any diff. (Menu->System->BootManager)
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Joined: 20 Jan 2006
Posts: 6759
Location: hobart
Posted: Sat 04 Apr 2009, 16:16
Post subject:
Plus it says
Another important note: This driver does not work on all Toshiba laptops, particularly those models which seem to have a BIOS or other firmware which was not developed by Toshiba itself. New reverse engineering work will have to be done on these machines, or Toshiba will have to disclose the necessary details. (For support of machines with Phoenx BIOS, try the [Omnibook driver].) The error you will see in this case is:
$ modprobe toshiba_acpi
FATAL: Error inserting toshiba_acpi
(.../kernel/drivers/acpi/toshiba_acpi.ko): No such device
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10 Discussion Questions for Book Clubs and Others
The Manny
By Holly Peterson
This readers' guide was not authorized or approved by the author, publisher or agent for the book. It is copyrighted by Janice Harayda and is only for your personal use. Its sale or reproduction is illegal except by public libraries, which may reproduce it for use in their in-house reading programs. Other reading groups that wish to use this guide should link to it or check the "Contact" page on One-Minute Book Reviews to learn how to request permission to reproduce the guide.
Five years ago Holly Peterson wrote a story about male nannies for the New York Times in which she explained why she had hired men to care for her 3-year-old son. It seems that Jack wanted to sell his baby sister at the supermarket. "Just leave her on the shelf next to the Teddy Grahams, Mom," he suggested. Peterson now returns to male nannies in her first novel, The Manny. Jamie Whitfield, a 36-year-old New York television producer, hires a younger man to care for her son because her rich, caddish husband doesn't seem to care that Dylan suffers from a "loss of self-esteem more than likely due to an absent dad." Jamie comes from a middle-class Midwestern background and loathes many of her "showy and vulgar" Upper East Side neighbors, whose sexual adventures can be as explicit as their preferences for brands like Bulgari and Chanel. And they aren't her only problem. The Manny also involves infidelity, a political scandal and an FBI investigation. As the action moves from Manhattan to Aspen, Jamie faces a final question: Should she stay with her indifferent husband or cast her lot with a seemingly penniless male nanny who has charmed her young son?
Questions for Readers
1. Many well-known novelists have written about the world of the Park Avenue elite, including Tom Wolfe in The Bonfire of the Vanities. What, if anything, did you learn from The Manny that you didn't get from other sources?
2. Nannies or other underlings have taken center stage in such recent bestsellers as The Nanny Diaries and The Devil Wears Prada. Some people would say that it's easier for a novelist to evoke sympathy for such obviously exploited characters than for their bosses. Jamie Whitfield is the boss in The Manny. Does Holly Peterson create sympathy for Jamie? What did you find appealing or not appealing about her?
3. Peterson says that Jamie comes from "middle-class, Middle American roots" and "married into" her elite realm on the Upper East Side of Manhattan. [Page 7] Did Jamie strike you as a credible daughter of the Heartland? Why or why not?
4. Jamie dislikes many of the people in her social orbit, whom she sees as pretentious snobs. She says that guests at a museum benefit are "showy and vulgar" and "unintellectual and boring." [Page 312] Does Jamie ever come across as a snob? Where? Do you think that Peterson intended this or that it's a flaw in the novel?
5. New York magazine had this novel reviewed by real-life manny, Jake Shapiro, who questioned its title: "A more apt title would be The Mommy – the book focuses pretty tightly on Jamie and her desires for happier kids, an exciting career, and a better marriage. Peter, the manny, is a stock character, a callow guy in his twenties on the rebound from a busted romance." ["A Man Among Nannies," by Jake Shapiro, New York, June 25, 2007 www.nymag.com/arts/books/features/33518/.] Do agree that Peter is a "stock character"? Why or why not? What could Peterson have done to make him less of a stock character and give him more depth?
6. One critic of The Nanny Diaries wrote that while the nanny and others in the novel were unique and believable characters, the boy the nanny cared for wasn't – he came across as a generic child. How well did Peterson portray Dylan in The Manny? Was he unique and believable or a generic boy?
7. Critics use the term roman-à-clef (novel-with-a-key) to describe books that invite you to guess which people or incidents inspired their characters. Does that characterization fit all or parts of The Manny? Why?
8. The Manny has its roots in an article Peterson wrote for the New York Times. A British reviewer wrote that the novel feels "more like a collection of newspaper pieces than a coherent narrative." [The Telegraph, March 18, 2007] Do you agree or disagree? What makes the book seem like a novel or collection of articles to you?
9. The Manny has multiple story lines that involve the manny, a political scandal Jamie is covering at her network, and an FBI investigation of the law firm where her husband, Phillip, practices. One challenge of keeping several story lines going is that you have to tie them together at the end. How well did Peterson do this?
10. Another challenge of working with multiple story lines that you have to give background for each up front, which can make a novel slow in getting off the ground. How would you describe the pace of The Manny? Did it ever seem to drag? Where? Why did the novel move faster in some places than others?
If you dare:
11. The Manny has some fairly explicit – some might say trashy – sex scenes, such as the one on page 167. Did these strike you as realistic? Or is Peterson one of those authors who should be barred by the New York City Council from ever trying to write a credible scene that includes the line, "Now she was on her knees …"
Vital statistics
The Manny. By Holly Peterson. Dial Press, 353 pp., $25. Published June 2007.
A review of The Manny appeared on One-Minute Book Reviews on June 26, 2007 https://oneminutebookreviews.wordpress.com/2007/06/26. It saved both with the June posts and in the "Novels" category on the site.
Links: The excerpt from The Manny appears on the online edition of Newsweek dated June 17, 2007. I can't link directly to it, but you can find the excerpt by Googling "The Manny + excerpt + Newsweek." You can also find an excerpt and more on the Random House site www.randomhouse.com.
Peterson's article "It's So Nice to Have a Manny Around the House" ran in the New York Times, Nov 3, 2002, pg. 9.2. You have to register for the Times's site to access the article but may be able to find it elsewhere on the Web.
Your book group may also want to read:
The Nanny Diaries. By Emma McLaughlin and Nicola Kraus. St. Martin's, 320 pp., $13.95 paperback (tie-in edition for the movie due out in September 2007). This novel does not have a diary format but uses first-person narration to depict the life of a nanny for ruthless parents who inhabit a world similar to that of The Manny.
Janice Harayda www.janiceharayda.com is an award-winning critic who has been the book columnist for Glamour, book editor of the Plain Dealer and a vice-president of the National Book Critics Circle. One-Minute Book Reviews does not accept free books from editors, publishers or authors, and all reviews and guides offer an independent evaluation of books that is not influenced by marketing concerns. If this guide helped you, please bookmark this site or subscribe to the RSS feed. Totally Unauthorized Reading Group Guides appear frequently but no on a regular schedule.
© 2007 Janice Harayda. All rights reserved.


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This is my winter look. I am a 13 year old "cockabishit" born in Calgary and now happily living on the Coast the past 10 years. I really dislike baths, people on skateboards, bikes and other things with wheels...its just wrong! My favorite things are mikey, my couch, beggin strips and walks with my family. Visit my profile to see my after picture!


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Author's Note: As of this writing, seminar marketing is working exceptionally well … if you get the pieces working together. I call these pieces the "Seminar Success Zone." The invitation is one piece. Please go to www.billgood.com/successzone. There you can listen to a conference call I did with an FA who raised $100 million in two years from seminar marketing.
A client sent me a seminar invitation and asked for a critique.
At best, it was awful. The worst was the title, which was undoubtedly a copyright violation.
Second worst: bullet points.
1) How a Seminar Invitation Works
When someone opens your envelope, they will first glance at the title. If it is boring, contains unfamiliar terminology, or otherwise fails to engage, the invitation is flying toward the waste can.
If the title is interesting, they will read the description, and then the bullet point.
The bullet points answer the question, "What will I learn from giving up two hours and missing the new episode of "CSI El Paso"?
Bullet points present the benefits someone expects to receive.
2) How to Write Bullet Points
Before I replied to my client, I posed the question: how do I teach him to write bullet points?
Then the fog lifted. My "bright idea muse" spoke: "Ommmmm. Go to Amazon and read reviews."
In 10 seconds or so I have found a book on the subject my client would be speaking on.
Behold! Benefits galore.
I emailed my client and told him: Read book reviews and then send me a revised invitation. In a couple of days, he returned the invitation. With a couple of very minor corrections, it was ready to go. He got it!
I had been able to teach how to write benefits.
3) How to Write for a Social Security Seminar
I decided to test the concept myself.
I Googled "Financial Advisor" + Seminar. The first thing that popped up was a lame announcement of a Social Security seminar. "Financial advisor hosts Social Security and finance seminar." No bullet points. Possibly someone attended.
Here's what I did.
Went to Amazon. Searched for "Social Security." Read reviews for the first three books. Took some notes. Wrote these benefits:
- Learn the basics as well as some advanced strategies.
- Shed light on a complicated topic.
- Clear up confusion on when to take your benefits.
- Revealed: Medicare premiums, co-pays and deductibles.
- What to do if you make a mistake.
- Untangle Medicare and its intricacies.
4) What to Learn From Book Reviews
Reviews are really answers to a survey, aren't they?
You could do a very expensive survey and ask, "What do you want to know about Social Security?"
Or, you could go to Amazon and read book reviews. There they tell you what people who found information were looking for.
It's magic.
This blog post is certainly not a complete course on writing seminar invitations. We're only dealing with Amazon magic tricks and bullet points.
Nevertheless, I would be remiss if I didn't strongly recommend: develop your invitation before you develop your handout and your slides.
The invitation tells you the topics for your seminar.
Once you know your topics, then you develop your handout. Now develop your slides to illustrate the most important points of in your handout.


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If you're looking for the perfect technology "coming of age" story (and who isn't?), Cambridge Investment Research just might have it.
When industry heavyweight Eric Schwartz founded the firm in 1992, the IT department consisted of a 16-year-old high school student.
"The kid would be at the office until midnight putting out a fire," Schwartz relates. "That's a lot of pressure. If he couldn't get it figured out, clients would not be able to trade the next day. Eventually his father came in and said it might be too much, and we agreed."
Enter Ryan Reineke, now the firm's senior VP of operations and technology. When Reineke joined the firm, it had just parted ways with the tech wunderkind and was in serious need of an upgrade, and upgrade it has.
"We're about to release WealthPort, a best of breed integration platform for the back office, as well as proposal generation and trading for the front office," Reineke told AdvisorOne at the 2013 FSI OneVoice Conference in San Diego on Tuesday. "It is a multi-custodian lead into UMAs and other offerings."
He added that competitors "have built the box," but Cambridge offers choice and flexibility across the platform.
"It offers things like model management, model trading and reporting. But it's fully scalable and can perform comprehensive book analysis."
Noting the conference panel which focused on technology trends for 2013 that occurred earlier in the day, Reineke rhetorically asked, "What is a mobile strategy? How do you define a mobile strategy with an advisor base that has incredibly different value propositions?"
He explained the Cambridge is in the process of answering that very question and coming out with a mobile strategy that is flexible enough for any advisor business model.
"It will be for the iPad first, and then be multiplatform supportable."
He added that an ongoing question involves the rollout of third party service providers within the broker-dealer.
"It ends up being a combination of building our own complex offerings in conjunction with offering the flexibility of outside products and services," Reineke concluded. "We want to make sure it is best of breed, but at the same time differentiated."
Cambridge recently launched eSignature capabilities for use with clients by advisors, powered by DocuSign. It's compatible with most desktop and mobile devices used by rep-advisors and their clients.
Check out complete conference coverage at AdvisorOne's FSI OneVoice 2013 enhanced landing page.


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Red Sox - 000 060 003 - 9 12 0With one out in the fifth, and the Royals having just taken a 2-0 lead, J.D. Drew singled to left. He would be the first of eight consecutive Boston batters to reach base off Hochevar.
Royals - 000 200 000 - 2 12 0
Alex Gonzalez singled to right, Jacoby Ellsbury tripled to left-center, tying the game at 2-2. Dustin Pedroia singled, giving him a 15-game hitting streak and putting the Sox up 3-2. Victor Martinez extended his streak to 22 games with a single to center. Kevin Youkilis walked, loading the bases. Jason Bay hit a first-pitch single to left, scoring two runs. David Ortiz followed with a first-pitch single down the right field line for the sixth run of the inning.
Mike Lowell had grounded out to short to begin the fifth. Now, as the tenth man to bat, he grounded into a 6-4-3 double play to end the rally. A reader named Dan left a comment on my 3 Outs In An Inning post from April:
Mike Lowell came close to making all three outs in the same inning tonight ... he was responsible for all three outs (although he did not represent all three). Has this happened before?What Lowell did was not all that unique. Now if he had made only the second out, and then the same eight Sox reached safely and then Lowell ended the inning with a third out in his third AB -- that would have been a first in major league history.
Beckett (6-12-2-1-7, 103) allowed a season-high 12 hits, but he stranded two Royals in each of the first four innings. And he was helped by a caught stealing in the fourth. After Martinez threw out David DeJesus, the next two batters singled, but were both left on base. His only perfect inning was the fifth.
Ortiz clocked a three-run dong to right-center in the ninth.
That is the magic number for both the Red Sox to eliminate the Rangers for the wild card and for the Yankees (who clinched a playoff spot last night) to win the AL East.
Pitchers for this weekend in New York:
Friday: Jon Lester / CC SabathiaOut West: Yankees/Angels at 3:30 and Rangers/A's at 10.
Saturday: Daisuke Matsuzaka / Joba Chamberlain
Sunday: Paul Byrd / Andy Pettitte


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Heligoland's rust-coloured sandstone cliffs jut dramatically out of the North Sea some 70 kilometres from the mainland. Blessed with a unique natural setting, the island also enjoys a mild maritime climate.
Although Heligoland is not strictly located on the high seas from a geographical or legal point of view, it is often referred to as Germany's only high seas island, due to its significant distance from the mainland. The island has good connections though, with boats travelling to it from Büsum, Hamburg, Cuxhaven, Bremerhaven and Wilhelmshaven. A particularly enjoyable way of making the North Sea crossing to Heligoland is to take a small cruise ship and see the majestic red cliffs rise up out of the water as you approach your destination. Heligoland has an interesting geological structure and is in fact an archipelago. The main island has three distinct areas: the lower, middle and upper lands, although the best spot for sunbathing is on the smaller island known as the Dune.
As there are no cars (and thus no exhaust fumes) on the island, Heligoland is an ideal destination for health and wellness holidays and for allergy sufferers, who will benefit from its fresh, virtually pollen-free North Sea air and mild maritime climate. Various themed trails guide holidaymakers through the island's flora and fauna to the world's smallest nature conservation area – the Lummenfelsen (guillemot cliffs). The charming Heligoland Museum showcases the island's history and culture. It is located in the Nordseehalle, a multi-purpose conference and events centre for business travellers.
Those seeking a real flavour of the island should make a trip to the heritage-listed fishermen's houses in the harbour, where they will get the chance to try a freshly caught local delicacy – the world-famous Heligoland lobster.
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