As a professional you need accurate and timely information to support your work managing our woods. We've compiled information and professional development opportunities to help you keep our forests healthy for generations.
Got VT Forester Licensing Questions?
Learn about the rules, read through the FAQs, and find all the forms needed to renew or apply for a forester license.
Connect landowners and clients to resources on ourVTwoods from anywhere through this share tool.
Get the latest updates on insect and disease observations, as well as overall forest health trends in VT.
Find professional development opportunities, stay informed on industry issues, and connect to other professionals.
Stay up to speed on the latest research and tools with through the Managing Our Changing Forests Webinar Series.
Learn about this new initiative to bring northeast foresters training to make sound, science-based decisions for forest ecosystem management, harvests and regeneration.
Check out these resources for guiding landowners through decision about the future of their land.
Find the information and forms you need to enroll and manage land in Vermont's Use Value Appraisal (UVA) Program.
Check out stumpage price reports and annual forest harvest reports.
Get tips to decrease your risk of infection from tick-borne diseases.


Montford Manor is a beautiful Arts & Crafts, newly constructed, Green-Certified home located on a quiet dead-end street and conveniently located to the vibrant downtown Asheville area.
Montford Manor has all the comforts of home and much more. All 4 bedrooms feature Serta I-Comfort adjustable beds (head and foot raise and lower). The master bedroom has a King size bed, all others are Queen size beds. While there are 4 beds to comfortably sleep 8 people, a Queen size sleeper sofa and comfortable Queen inflatable bed are also available for additional guests. 3 bedrooms have cable connected smart TVs. There are 3 full bathrooms (one with a tub). The master suite has it's own private bathroom. 2 bedrooms upstairs share a bathroom. The bedroom downstairs has a full bathroom nearby.
The kitchen is fully equipped with modern appliances, utensils, cookware and bakeware to prepare home cooked meals. A gas grill is on the outdoor deck, located just outside of the kitchen.
High Speed internet is available via WiFi throughout the house. Relax and enjoy the fresh mountain air on our rocking chairs on the wrap around front porch or on one of the 2 outside decks. Take advantage of our high efficiency washer and dryer to wash your clothes before returning home. There is one parking space and street parking available.
Downtown can be reached 20 minutes on foot or 5 minutes by car. The Asheville Visitors Center is a short walk away (10 minutes), where you can book anything from tickets to Biltmore House or zip lining and white water rafting, or take a lovely "Hop On/Hop Off" trolley tour. There are restaurants and coffee shops within walking distance as well. The nearest grocery stores (Harris Teeter and Trader Joes) are just a 5 minute drive away. Montford Manor is located just 20 minutes from the Asheville Regional airport. The home has convenient access to I-26, I-40, and I-240.


text:
Mauro Geraldo Galvão, mais conhecido como Mauro Galvão (Porto Alegre, 19 de dezembro de 1961), é um ex-futebolista e técnico brasileiro que atuava como zagueiro.

Carreira

Como jogador
Mauro começou a carreira profissional jogando no clube que torcia na infância , o Internacional, e com apenas 18 anos, ajudou o clube a conquistar de forma invicta o Campeonato Brasileiro de 1979. Pelo Internacional foi ainda tetracampeão gaúcho (1981-1984), campeão do Torneio Heleno Nunes (1984) e, juntamente com todo o elenco do clube, mas com a camisa da Seleção Brasileira, conquistou a medalha de prata nas Olimpíadas de 1984. Durante este período, Mauro Galvão se tornou um dos 10 jogadores que mais vestiram a camisa do Internacional na história.

Após sete anos a serviço do Internacional Mauro Galvão transferiu-se para o Bangu, aceitando o convite de Paulo César Carpegiani para um projeto para a conquista do Campeonato Brasileiro de 1986. Apesar do ambicioso projeto e com o grande investimento do clube carioca, a equipe não alcançou o título.

Mas o ano de 1986 não foi apenas de tristeza para Mauro Galvão que foi pela primeira vez chamado para o elenco principal da Seleção Brasileira e fez parte do grupo chamado para a disputa da Copa do Mundo daquele ano.

Em 1987 Mauro Galvão transferiu-se para o Botafogo, ao lado de Marinho e Paulinho Criciúma. Na verdade, eles quase foram para o Fluminense, que pagaria por eles os 35 milhões de cruzados que o Botafogo iria pagar ao rival pelo passe de Jandir. Mas quando a diretoria do Botafogo ficou sabendo dessas intenções desistiu de comprar o passe de Jandir e trouxe os três jogadores do Bangu. Em General Severiano, Mauro Galvão ajudou o clube carioca a conquistar contra o Flamengo o Campeonato Carioca de 1989 após 21 anos sem títulos.

Três anos atuando pelo Botafogo valeram a Mauro Galvão uma vaga na Seleção Brasileira que disputou a Copa do Mundo da Itália em 1990. Mauro Galvão foi um dos três jogadores escolhidos por Sebastião Lazaroni para formar a defesa brasileira num esquema tático que não agradou aos torcedores.

A seleção foi eliminada pela Argentina ainda nas oitavas-de-final, mas Mauro Galvão terminou a Copa do Mundo com boas atuações que renderam-lhe uma proposta do Lugano, da Suíça.

Mauro Galvão passou seis anos na Suíça até que em 1996 aceitou a proposta do Grêmio, e retornou ao Brasil, conquistando o Campeonato Brasileiro de 1996 e a Copa do Brasil de 1997 pelo tricolor gaúcho.

Em 1997 aceitou um novo desafio e transferiu-se para o Vasco da Gama, conquistando no mesmo ano o seu terceiro título do Campeonato Brasileiro. Permaneceu no Vasco no ano seguinte para dar continuidade ao projeto do centenário do clube que visava a conquista da Libertadores de 1998 e da consequente disputa da Taça Interclubes. O objetivo inicial foi alcançado e Mauro Galvão como capitão da equipe levantou pela primeira vez na sua carreira a taça de campeão da Libertadores da América, mas na disputa da Taça Interclubes o Vasco foi derrotado pelo Real Madrid, e deixou escapar o título inédito.

O sucesso no Vasco fez Mauro Galvão permanecer no clube até o fim da temporada de 2000, onde ainda conquistou os títulos do Torneio Rio-São Paulo em 1999 e da Copa Mercosul e do Campeonato Brasileiro em 2000. No início da temporada de 2001, ele retornou ao Grêmio para encerrar a carreira e ainda conquistou o Campeonato Gaúcho de Futebol de 2001 e a Copa do Brasil de 2001.

Em 2002, aos 40 anos de idade, após a disputa de mais uma Taça Libertadores, Mauro Galvão decidiu encerrar a sua vitoriosa carreira.

Como técnico
Um ano após encerrar a carreira de jogador, Mauro Galvão foi convidado pelo Vasco da Gama para ser o treinador principal da equipe. O desafio foi aceito e iniciou-se então a carreira de treinador.

Após um curto período como treinador principal, ele assumiu o cargo de assistente de treinador no próprio Vasco até o início da temporada de 2004 quando foi contratado pelo Botafogo para ser treinador, onde também já tinha atuado como jogador na década de 1980.

No início de 2005, ele assumiu o Náutico onde permaneceu por seis meses.

Como diretor-executivo de futebol
Mauro Galvão começou a carreira de diretor-executivo de futebol no . Assinou contrato e foi apresentado à imprensa e à torcida. Ele chegou para substituir Rodrigo Caetano. Novo no cargo, Galvão relatou que acompanharia o grupo profissional e, posteriormente, as categorias de base do clube.

Demitido do tricolor no decorrer da temporada, o ex-zagueiro acertou com o  para comandar a gestão de futebol de 2010. Porém, seis meses depois, não agradando aos dirigentes do clube, foi demitido.

No dia 8 de dezembro de 2010, Mauro Galvão foi anunciado como o novo superintendente de esportes do , com a missão de montar o elenco do time para a busca do tricampeonato estadual e das disputas da Copa do Brasil e do Campeonato Brasileiro. Após não ter alcançado os objetivos do clube, foi anunciado o desligamento de Mauro Galvão do Avaí no dia 24 de agosto de 2011.

Livro
Em 1998, Mauro Galvão lançou a sua biografia intitulada "Mauro Capitão Galvão - Lições de Vida, Lições de Futebol", que mostra imagens, histórias, estatísticas e curiosidades da sua carreira até aquele ano. Uma das curiosidades sobre a carreira de Mauro Galvão é que ele é o jogador que conquistou dois campeonatos brasileiros com o maior intervalo de tempo entre ambos, 17 anos. O primeiro em 1979, pelo Internacional, e o segundo em 1996, pelo Grêmio.

Títulos
Internacional
 Campeonato Brasileiro: 1979
 Torneio Heleno Nunes: 1984
 Campeonato Gaúcho: 1981, 1982, 1983 e 1984

Bangu
 Taça Rio: 1987

Botafogo
 Campeonato Carioca: 1989 e 1990
 Taça Rio: 1989

Lugano
 Copa da Suíça: 1992-93

Grêmio
 Campeonato Brasileiro: 1996
 Copa do Brasil: 1997 e 2001
 Campeonato Gaúcho: 2001

Vasco da Gama
 Copa Libertadores da América: 1998
 Copa Mercosul: 2000
 Campeonato Brasileiro: 1997 e 2000
 Torneio Rio-São Paulo: 1999
 Campeonato Carioca: 1998
 Taça Guanabara: 1998 e 2000
 Taça Rio: 1998 e 1999
 Troféu Bortolotti (Itália): 1997
 Seleção Brasileira
 Copa América: 1989

Prêmios Individuais
 Bola de Prata da Revista Placar: 1979, 1985 e 1997

Ligações externas
 Perfil de Mauro Galvão  em soccerway

Naturais de Porto Alegre
Futebolistas do Rio Grande do Sul
Futebolistas do Club de Regatas Vasco da Gama
Futebolistas do Botafogo de Futebol e Regatas
Futebolistas do Grêmio Foot-Ball Porto Alegrense
Futebolistas do FC Lugano
Futebolistas do Bangu Atlético Clube
Futebolistas do Sport Club Internacional
Futebolistas nos Jogos Olímpicos de Verão de 1984
Medalhistas olímpicos de prata do Brasil
Jogadores da Copa do Mundo FIFA de 1986
Jogadores da Copa do Mundo FIFA de 1990
Jogadores da Seleção Brasileira de Futebol
Treinadores de futebol do Rio Grande do Sul
Treinadores do Botafogo de Futebol e Regatas
Treinadores do Club de Regatas Vasco da Gama
Dirigentes do Avaí Futebol Clube
Dirigentes do Grêmio Foot-Ball Porto Alegrense
Treinadores do Clube Náutico Capibaribe
Dirigentes do Club de Regatas Vasco da Gama

redpajama_set_name: RedPajamaWikipedia


Producer Pro has everything a carrier needs to automate and simplify producer management.
Improve efficiency, maintain compliance, and reduce risk for your organization.
It's time consuming to manage producer compliance profiles, changing roles, and relationships. Consolidate and capture all relevant information about captive or independent agents over the entire business lifecycle and share it easily with downstream distribution systems. Leverage one source of accurate up-to-date information including single producer identifiers, book of business management, continuing education records, and more.
Reduce manual data entry and connect with all the data sources you need to manage compliance. With regular software updates from CallidusCloud, you will reduce risk and keep up with regulatory changes. Use turnkey data synchronization with NIPR, DTCC, FINRA, and other regulators and monitor licenses, appointments, education/certifications, background checks, credit checks, and previous employment history—all while capturing the changes made for detailed audit logs.
A single repository for producer information allows you to see the key information you need, when you need it. Gain a historical view of producers with insights to save time and money. Have complete visibility into every producer, book of business, vendor, customer, geographical area, policy, product, and more. Use out-of-the-box graphical reports to simplify planning and compliance and build custom reports and KPIs.
Not being able to connect systems creates redundant data sources that increase operation costs and introduce errors. Producer Pro easily integrates with on-premise and SaaS solutions using batch utilities or real-time REST-based web services. Leverage accurate and current data in Producer Pro while maintaining existing systems.
Meeting your unique requirements shouldn't require complex coding. Based on a proven cloud infrastructure, Producer Pro is built for insurance-industry business users. Without coding, users can add, move, or change fields; control the look and feel of all screens, including branding and layout; design and generate reports; define code values, security, defaulting logic, workflow, and more; and add and change hierarchies.
Grappling with the DOL Disruption?
Schedule your custom demo with a Producer Pro expert now.


Ella ella don omar ft zion y lennox download. Musicians and groups are pa Rantsila - Lassi - Ilona - Nick Lowe - Eino Valtanen - Essi Wuorela - Lauluyhtye Rajaton - O- zone - Escobar - Renegades - Ella ja Aleksi - Sir Elwoodin Hiljaiset Värit - Il Divo - Värttinä - Äimä - Method Man - Air - Robin Williams - Mud - Dr. This is a complete alphabetical list, as of December.
Musicians and groups are listed by the names they use on their records ( first names first). Watch breaking news videos whether it' s a landline , viral videos , cell phone number, the location, original video clips on o searches thousands of sources across 12 billion public records to look up the most recent owner of that number even the carrier if available. As of march this website contained profiles of 8 600 musicians. Feelgood - David Hasselhoff - Fredi - Isto Hiltunen - Nina Hagen - Nits - Trio Töykeät - Tom Jones - Elvis - Sheena Easton - Nat King Cole.
Spokeo is a people search engine that organizes white pages listings social network information into simple profiles to help you safely find , public records learn about people.
Meet the Orphans is the fourth studio album by reggaeton artist, Don Omar, released on November 16,. The album features the artists under the " Orfanato Music Group" label and other reggaeton artists. The album includes the promotional single " Hasta Abajo" and the album' s lead single " Danza Kuduro" featuring French- born Portuguese singer Lucenzo, as well as collaborations from Don Omar' s. Download Album: Wisin - Victory ( ) J Lanny Ft.
Paulino Rey, Chris Wandell, Green Cookie y Joyce Santana – Mi Jeva.
El interprete de " Sed" se ha acercado a contarnos todo lo bueno que está pasando en su carrera. " Termine el año compartiendo tarima con jhay Cortez en Funky Night Club, Capsulon Party ( evento creado por la reconocida marca Moña ) y cante en Las fiestas de las Calle San Sebastián en La. MARCELLO BALLROOM, LEVEL 4 Up until two years ago, a music video was used to promote the song. With the advent of different social media and streaming platforms, it.
30 Exitos Que llegan al Alma De - Teodoro Reyes ( Direct MP3 link) 30 Exitos Que llegan al Alma De - Teodoro Reyes ( Direct MP3 link). El novel cantante Yoi Carrera firmó ayer, miércoles, con la compañía Fresh Productions de Juan Orengo ( Yomi Fresh).
Fresh Producctions desarrolló la carrera de Wisin y Yandel con sus primeras producciones " Los Reyes del Nuevo Milenio ( ) ", " De Nuevos a Viejos ( ) " y " De Otra Manera ( ) ". is and in to a was not you i of it the be he his but for are this that by on at they with which she or from had we will have an what been one if would who has her. Watch breaking news videos, viral videos and original video clips on o is one of the nation' s most trusted sites for uncovering scammers, telemarketers, criminals, and catfishers.


They say in the finance industry that past performance is not necessarily indicative of future results. In politics, you can almost always drop the "not." The past tells us what Republicans are prone to do when in January, a new crop of GOP legislators come to Washington and take the gavel of both houses of Congress.
The last times Republicans controlled both Houses of Congress were 2003-2005 and 2005-2007. The signature legislation of those eras were the Medicare Prescription Drug Benefit in the 108th Congress and then the lack thereof of the pork barrel-filled "Do Nothing Congress" in the 109th.
One of the best, but little noted things that happened was the cutting of taxes for the middle class. Despite it being very good for the economy, it is rarely mentioned because of the economic collapse of 2008 that each party has tried to cast the blame on the other for.
After those four years Republicans lost control of both houses of Congress for the 110th Congress (2006 election) and then lost the Presidency two years later.
There are two lessons to be learned for the new GOP majority. And that is to avoid to being known for 1) the largest expansion of government spending since the Great Society program, and 2) doing nothing. Those four years Republicans basically became Democrats when it came to spending. They brought home the bacon, appropriation bills were filled with pork, and the Medicare Prescription Drug bill was a monstrosity.
The GOP has been granted a second chance after the November 2014 elections. If we want to lose our majorities again and help elect Hillary Clinton or whoever the Democrats decide to crown in 2016, the quickest way for us to do that is to spend like drunken sailors like we did last time we controlled both houses of Congress and get nothing else done.
What should we be doing? Tax reform. Border Security. Defeating ISIS. Lower the corporate tax rate. Regulatory reform both for small business and to make it easier for businesses to access capital. Dodd Frank Reform. Open up American energy and pass energy bills under the guise of jobs bills. Crack down on the IRS and the NSA. Repeal sections of the Patriot act. Defund the DOJ. The opportunities to fix this Country are endless and for once Congress can look like heroes to the public.
What should we not be doing? NOTHING for fear that the President will veto. Let him and when he does make sure every Communications staffer on the Hill pushes the veto to every media outlet large or small. I would love to see a wall on the new Majority Leader McConnell's wall which is covered in all of the legislation that the President vetoed. Let Obama veto most of them, then he will be the Do Nothing President. Hillary will inherit his obstructionism and the GOP will have something to demonstrate they were adults in office and deserve to stay in the majority.
Just as dangerous however is divisive rhetoric within our own Party. Right now the Democrats realize their charade is up however and they realize the only way they can win is by running a campaign based on emotions and facts and make sure the GOP is divided. Comments from the newly announced director of the NRSC Ward Baker were an example of the mindless aspersions that Washingtonians feel the need to cast in the direction of tea party and constitutional conservatives: "We said we were going to be the Nick Saban of recruiting, we were going to recruit the best candidates, put them in the right position. We decided we couldn't be Akin-ed anymore. No more witches, no more gaffes." These need to be erased from any conversations happening both internally and in the public eye.
Truth is, the 2014 election cycle has taught us within the GOP that neither the establishment nor the grassroots are strong enough to be on their own. Neither side can declare a total victory as both groups won and lost different races. Together as a team we won and beat the Democrats.
Maybe it's naïve. Maybe it's innocent. But in 2015, Republicans have a chance to buck the trends of their abysmal past performance. If we continue the unity, respect the various viewpoints within our Party and work together, we can reclaim the White House in 2016 and establish a long-term majority dedicated to reducing the size of government.


text:
Online TV services offset cord cutting losses in Q3
Nov. 21, 2017, 9:32 AM
Online TV services including Sling TV and Playstation Vue added 962,000 subscribers in Q3 2017, which helped offset the 872,000 in subscriber losses traditional pay-TV providers experienced in the quarter, according to research firm MoffetNathanson, per Fierce Cable.
When factoring in online TV subscriber additions, the US pay-TV ecosystem added 90,000 subscribers in Q3 2017, up from a net loss of 275,000 in Q3 2016.
Though the nearly one million online TV service subscriber additions is promising, players in the pay-TV ecosystem still have reason for concern:
This year has already seen more cord-cutting losses than all of 2016. The 872,000 in subscriber losses represents a 3.1% year-over-year (YoY) increase from 559,000 in Q3 2016. Roughly 2.6 million consumers cut the cord in the first three quarters of this year, while roughly 1.7 million did in 2016. The increase could be partially attributed to video streaming services like Netflix aggressively broadening content libraries, which may have made traditional TV less of a necessity for some consumers.
Online TV service subscriber additions are not benefitting all TV networks equally. Disney, NBCUniversal, CBS, and Fox are in nearly every online TV bundle. Conversely, Discovery, A&E Networks, Scripps, and Viacom, and independent networks are in less than 50% of online TV services. Those networks left out of online TV bundles could partner with each other. By pooling their programming together, they could propose a more compelling and cheaper offering to bundle operators.
And pay-TV subscriber losses could be worse than MoffetNathanson's estimates.Kagan estimated total subscriber losses for Q3 2017 at 1.2 million, when factoring in losses of smaller cable companies, while Leichtman Research Group pegged total losses at 943,000. Regardless, it's clear that analysts agree that cord cutting is accelerating in 2017.
The revenue lost from cord cutting is projected to be greater than online TV service revenue. Online TV services typically are priced at about $30-$40 per month, while traditional cable packages cost about $100. While some cord cutters are captured by digital streaming services, media companies will lose over $13 billion in revenue over the next 10 years, according to Barclays cited by Bloomberg.
More: BI Intelligence BI Intelligence Content Marketing Digital Media Cord Cutting

redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Xamarin.Android always getting previously selected Language and not current I am developing an app in Xamarin.Android and I am fetching the current system language using
CultureInfo.CurrentUICulture.TwoLetterISOLanguageName;

It returns the current system language but when I close the app and go to settings and change the language to some another and again open the app then it still returns the old language only. When I re install the app it then shows me the new language.

A: I created a simple xamarin.android project and as I explained in the comment, I put the CultureInfo.CurrentUICulture.TwoLetterISOLanguageName; in the OnResume() method.Then I start the app, go to the settings app to change the language, then open the app again, it returns the old language. But if I make the app stop by slide it out of the task stack, then open the app again, it returns the new language.
The code is like this:
public class MainActivity : AppCompatActivity
    {
        TextView tv;
        protected override void OnCreate(Bundle savedInstanceState)
        {
            base.OnCreate(savedInstanceState);
            // Set our view from the "main" layout resource
            SetContentView(Resource.Layout.activity_main);
        }

        protected override void OnResume()
        {
            base.OnResume();

            var lang = System.Globalization.CultureInfo.CurrentCulture.TwoLetterISOLanguageName;
            Log.Debug("OnResume", lang);

            tv = FindViewById<TextView>(Resource.Id.textView1);
            tv.Text = lang;
        }
    }

redpajama_set_name: RedPajamaStackExchange


text:
<?php
namespace Concrete\Core\Express\Form\Context;

use Concrete\Core\Entity\Express\Control\Control;

class FormContext extends Context
{

}

redpajama_set_name: RedPajamaGithub


text:
Rockstar Co-Founder Dan Houser Has Seemingly Started a New Studio
Dan Houser is on the ground floor of Absurd Ventures in Games
byMatt T.M. Kim
Posted July 2, 2021, 2:39 a.m.
Rockstar Games co-founder and Grand Theft Auto writer, Dan Houser, has seemingly started up a new video game company studio.
As spotted by Rockstar Mag a new company started in the United Kingdom called Absurd Ventures In Games has recently been registered. According to a business listing, Dan Houser is involved with Absurd Ventures in Games as Director.
Details about the new company are sparse. Absurd Ventures in Games was incorporated in the UK on June 23, 2021, and is classified as a "Ready-made Interactive leisure and entertainment software development" company.
However, given how few details there are it's not necessarily the case that Absurd Ventures in Games is a new game development studio or a different company working in the games industry.
In 2020 Dan Houser left Rockstar Games, the company he helped found in 1998 with his brother Sam. Rockstar parent company Take-Two Interactive confirmed Dan Houser left in 2020 and issued a statement thanking Houser for his years of service. Sam Houser remains at Rockstar Games as president of the company.
Houser is best known for his work on Rockstar's many critically acclaimed games and served as a writer on almost all of the company's Grand Theft Auto and Red Dead Redemption titles. The last Rockstar Games release was Red Dead Redemption 2, one of the most critically acclaimed games of 2018.
Meanwhile, the internet continues to be obsessed over when Grand Theft Auto 6 will come out.
Matt T.M. Kim is IGN's News Editor.
Developer: Rockstar Studios
Publisher: Rockstar Games
Release Date: Oct. 26, 2018
Platforms: PlayStation 4, Xbox One, Stadia, Pc
2 months Comments
Red Dead Redemption 2 Is More Popular Than Ever on PC
2 months, 3 weeks Comments
The 10 Best-Selling Video Games of All Time
12 Dream Video Game Movies and TV Shows


This city centre hotel has a great location close to Palma´s bars and restaurants and is home to a renowned jazz club. Its well-equipped business centre is equipped with computers with Internet access, printers, copiers, scanner and secretarial services. The hotel has two small-scale meeting rooms, accommodating 12 - 25 people depending on layout, with state of the art audio-visual media conferencing.


text:
Phaendin Thong railway station is a railway station located in Nong Yai To Subdistrict, Chai Badan District, Lopburi Province. It is a class 3 railway station located  from Bangkok railway station.

References

Railway stations in Thailand
Lopburi province


I did a random poll of an 8th grade class last month. All but one student in the class knew about the popular social networking site, all but she had visited this popular teen hang-out, and five of the students in the class had their own accounts. I did not ask if they were over 14, the magic age for use of the site.
One of the middle school guidance counselors came to see me and wants to set up an informational workshop for parents to let them know how these social networking sites work, and, more importantly, how much information about their child could potentially be being shared with the world. We have already drafted a letter to the middle school parents and sent it home, and are in the process of creating one for high school parents.
The parent education piece is not new for us. We have held instant-messaging workshops, to help parents keep their children safe, and also host a district safety page for parents.
Here is another good article from a Lehrer Newshour Special with students which aired this week.
Does anyone have any material they have developed for their school or district which they would like to share?


text:
Q: Nextjs public folder with next-routes not working did anyone get the public folder working with custom express server and next-routes? getting 404 errors for all assets in public/asset
repo- https://github.com/msreekm/next9-custom-server-routes-example

A: There is a warning not to use static folder. If you will change from static to public you should change like this:
FROM
static/images/javascript-logo.png

TO
public/images/javascript-logo.png

OR
You should create public folder in root dir. Then you should move static folder to public folder. There will no need to change anything where it is used.

A: Nested public folders seem to be completely broken in latest NextJS. I'm personally switching back to static.


text:
Records and Confidentiality
Certain items of information about individual students are fundamental to the educational process and must be recorded. This recorded data is used for only clearly defined purposes and is safeguarded and controlled to avoid violations of personal privacy.
SPU has the responsibility to effectively supervise any access to and/or release of official information about its students. In this regard, SPU is committed to protecting the right of privacy of all individuals about whom it holds information, records, and files. Access to such records is restricted to the student concerned, to parents of a dependent student, to others with the student's written consent, to officials within the University, and to a court of competent legal jurisdiction.
The following policies have been established to comply with the Family Educational Rights and Privacy Act of 1974 (hereafter referred to as the "Act"):
The Act provides that public "directory information" about a student may be made available to third parties without permission of the student. However, public notices must be given of intent to publish the information, so that those students wishing to withhold information from public access (such as an unlisted telephone number) may do so.
With the exception of directory information, no information in any student file may be released to any individual or organization without prior written consent of the student. When disclosure of information is mandated by court order or subpoena, the staff member receiving such orders must immediately notify in writing the student concerned, prior to compliance with the legal order.
Information from University records about students is released for approved research purposes only if the identity of the student involved is fully protected.
With certain exceptions, official student information collected and maintained by SPU is available for inspection and review at the written request of the student. Clarification of exceptions may be obtained by contacting the university registrar.
A request for general access to all official records maintained by the University must be made in writing to the university registrar. A request for access to information maintained by a particular office may be addressed to the administrative head of that office. When making such a request, the student must provide proper identification.
The designated staff person must supervise the review of the contents of the record with the student. The student is free to make notes concerning the contents, but no material may be removed from the record. Student requests for access to appropriate information must be granted within 45 days of the written request.
If health reasons or extreme distance from the University prevent the student from inspecting the education record, then copies of specific education records will be made. The student must pay all copying expenses in advance of release of the record. Unless stipulated otherwise in the University's current Graduate Catalog, all copies are 25 cents per page.
The University allows any enrolled student the option of becoming confidential in the computer system to protect his or her identity from outside sources.
A request for confidentiality must be submitted in person to Student Academic Services. When an SPU student requests their records and identity to be flagged as confidential, the following ramifications may apply:
The University will respond to inquiries about the confidential student as though the student is not known at the University.
The confidential student may not obtain any information about records over the telephone, but must appear in person with proper identification to make any inquiry.
The confidential student will not appear in any student publications or listings, including, but not limited to, the Commencement brochure and the online directory.
Student loan agencies may have difficulties accessing information necessary to carry out their functions. Since the University will not be able to confirm attendance, the confidential student's loans could possibly be placed into repayment status.
A student graduating from the University should remove the confidentiality status at the time of graduation or at the time he or she leaves the University.
If the confidentiality status is not removed, the student may have difficulty obtaining information, and staff may be unable to identify them quickly or easily.
If the confidentiality status is not removed, this confidential status could prevent future employers from gaining access to educational records.
Students who wish to remove their confidential status must come in person to Student Academic Services with proper identification.
Student correction of education records
A primary function of the Registrar's Office is to uphold academic integrity by ensuring that records of a student's course registration, course completion, and grades are accurate and comprehensive. Therefore, academic history data are not subject to erasure by request under the European Union General Data Protection Regulations or any other regulation.
Students who believe that information contained in their education records is inaccurate, misleading, or violates privacy or other rights, may request that the University amend the records. The first step is to contact the University registrar or records custodian.
The University will decide within a reasonable period of time whether or not to do so. If the University declines to amend the student's records, it will inform him or her of the right to a hearing. Upon written request, the University will provide an opportunity for a hearing to deliberate the student's case. However, a hearing may not be requested by a student to contest the assignment of a grade.
If the hearing panel determines that the student's challenge is without merit, the student may place in his or her record a statement commenting upon the information and setting forth reasons for disagreeing with the University's decision. A complete copy of the University's FERPA policy may be obtained here or by contacting the dean of student life or SAS.
Students have the right to file complaints concerning alleged failures by the University to comply with the requirements of the Act. Such complaints should be addressed to:
Family Educational Rights and Privacy Act Office (FERPA)
U. S. Department of Education
400 Maryland Ave. SW


text:
Yanbal es una compañía multinacional peruana de fabricación y venta directa de productos de belleza y cosméticos. Fue fundada en Lima, Perú, en 1967.

Historia

La compañía fue fundada en Perú en el año 1967 por los hermanos Fernando y Eduardo Belmont Anderson. La empresa tuvo éxito y poco después de 1981 comenzó la expansión internacional en Colombia y México. Se dividió en 1988, cuando cada uno de los hermanos decidió emprender su propio negocio, quedando a cargo Fernando en Yanbal.

En 2004 se construyó una nueva fábrica para la operación de la marca Unique. En 2011, su hija Janine Belmont  se hizo cargo de la presidencia de la empresa.

Gestión

La compañía se basa en la venta de productos de belleza por catálogo. Sus principales competidoras son Belcorp, la empresa fundada por Eduardo Belmont, y la marca brasileña Natura. A 2018, la empresa tiene presencia en 10 países: Perú, Colombia, Ecuador, Bolivia, Guatemala, México, España, Italia, Estados Unidos y Venezuela. En 2011, tuvo ventas estimadas en $720 millones de dólares. Forbes estima que el 95% de la compañía se encuentra en poder de Fernando Belmont.

Véase también
Belcorp
Le Noche Doré

Referencias

Enlaces externos
Web de la compañía
Yanbal cumple 50 años

Empresas fundadas en 1967
Empresas de cosmética de Perú
Empresas de Perú


Siri Singh Sahib Bhai Sahib Harbhajan Singh Khalsa Yogiji, also known as Yogi Bhajan was the chief religious and administrative authority for the Ministry of Sikh Dharma in the Western Hemisphere. A deeply devoted Sikh, his inspiration and example motivated thousands to embrace the Sikh way of life. Through his personal efforts, Sikh Dharma was legally incorporated and officially recognized as a religion in the USA in 1971.
Yogi Bhajan was a Master of Kundalini Yoga, the Yoga of Awareness, and a dedicated and inspired teacher. Since arriving in the United States in 1969, he dedicated himself to bring meaning, dignity and a reconnection of Spirit into the lives of people everywhere. As he worked diligently to spread the science and practice of Kundalini Yoga throughout the Western Hemisphere and beyond, Yogi Bhajan became widely recognized as a world leader and champion of world peace and healing.
Throughout recorded history, a handful of spiritual giants have arisen as dynamic catalysts for the advancement of human consciousness. Their revolutionary teachings and their very presence on the planet have accelerated the progress of millions of souls. Such a master, a Teacher of teachers, was Yogi Bhajan.
Yogi Bhajan left his physical body on October 6, 2004. However, the legacy of his teachings and his inspiration live on and the light of his spiritual essence continues to shine and to bless the entire humanity.


text:
Tobacco Smoke Induces Urokinase-Type Plasminogen Activator and Cell Invasiveness: Evidence for an Epidermal Growth Factor Receptor–Dependent Mechanism
Baoheng Du, Helen Leung, K.M. Faisal Khan, Charles G. Miller, Kotha Subbaramaiah, Domenick J. Falcone and Andrew J. Dannenberg
Baoheng Du
Helen Leung
K.M. Faisal Khan
Charles G. Miller
Kotha Subbaramaiah
Domenick J. Falcone
Andrew J. Dannenberg
DOI: 10.1158/0008-5472.CAN-07-1388 Published September 2007
Multiple tobacco smoke–related premalignant and malignant lesions develop synchronously or metachronously in various organ sites, including the oral cavity. Both field cancerization and clonal migration seem to contribute to the occurrence of multiple tumors. Although the importance of endogenous factors (e.g., oncogenes) in regulating clonal migration is well established, little is known about the role of exogenous factors. Hence, the main objective of this study was to elucidate the mechanism by which tobacco smoke stimulated the migration of cells through extracellular matrix (ECM). Treatment of MSK-Leuk1 cells with a saline extract of tobacco smoke induced the migration of cells through ECM. Tobacco smoke induced the expression of urokinase-type plasminogen activator (uPA), resulting in plasmin-dependent degradation of ECM and increased cell migration. AG1478, a small-molecule inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase, a neutralizing antibody to EGFR, or an antibody to amphiregulin, an EGFR ligand, also blocked tobacco smoke–mediated induction of uPA and cell migration through ECM. PD98059, an inhibitor of mitogen-activated protein kinase (MAPK) kinase activity, caused similar inhibitory effects. Taken together, these results suggest that tobacco smoke activated the EGFR→extracellular signal-regulated kinase 1/2 MAPK pathway, causing induction of uPA. This led, in turn, to increased plasmin-dependent degradation of matrix proteins and enhanced cell migration through ECM. These data strongly suggest that chemicals in tobacco smoke can mimic the effects of oncogenes in regulating uPA-dependent cell invasion through ECM. These findings also strengthen the rationale for determining whether inhibitors of EGFR tyrosine kinase reduce the risk of tobacco smoke–related second primary tumors. [Cancer Res 2007;67(18):8966–72]
clonal migration
Multiple premalignant or malignant lesions can develop synchronously or metachronously in the oral cavity, urothelial tract, and respiratory epithelium ( 1– 5). One possible explanation for this phenomenon is field cancerization ( 6). According to this concept, multiple lesions arise because the entire field (e.g., aerodigestive tract) was chronically exposed to carcinogens, such as those in tobacco smoke. In this instance, carcinogens affect the epithelium at multiple sites, leading to numerous mutations and independent growth of multifocal unrelated tumors. However, the independent origin of some second primary tumors (SPT) has been challenged. For example, genetic evidence has suggested a common clonal origin of multiple bladder tumors ( 1, 2). In addition, studies have suggested that SPT in the head and neck can be a consequence of clonal spreading rather than development of independent lesions ( 3, 4). In the oral cavity, clonal spreading of both invasive cancer and noninvasive leukoplakic lesions has been described ( 3, 4). Hence, it seems that both field cancerization and mucosal spreading of clonal cells contribute to the occurrence of multiple tumors. Although the mechanisms underlying field cancerization are well characterized, very little is known about the factors that contribute to clonal migration.
One of the key steps in cell migration is degradation of the extracellular matrix (ECM). Several lines of evidence suggest that the serine proteinase urokinase-type plasminogen activator (uPA), together with its high-affinity receptor, uPAR, is important in initiating a proteolytic cascade that stimulates cell migration ( 7– 12). uPA cleaves the Arg560-Val561 bond of plasminogen, thereby generating plasmin, a serine proteinase with wide substrate specificities ( 13). uPAR helps to localize plasminogen activation to the cell surface and uPA bound to uPAR is relatively resistant to inhibition ( 14, 15). Plasmin binds to and degrades several components of the ECM, including the adhesive glycoproteins, fibronectin, and laminin ( 16– 18). Moreover, plasmin activates several members of the metalloproteinase family, which degrade collagenous and noncollagenous ECM components ( 19). Activation of this proteolytic cascade has been implicated in processes requiring cell migration, including inflammation, wound healing, and cancer metastasis ( 20– 24). As detailed above, clonal spreading occurs in smoking-related neoplasia but the effects of tobacco smoke on either cell invasiveness or the uPA-uPAR-plasmin axis are unknown.
In the present study, we first determined that exposure to tobacco smoke extract stimulated the invasiveness of oral leukoplakia cells. Subsequently, tobacco smoke was found to stimulate cell invasion by inducing the expression and release of uPA, leading, in turn, to plasmin-mediated degradation of ECM. Finally, we showed that tobacco smoke–mediated induction of uPA was a consequence of activation of epidermal growth factor receptor (EGFR)→extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) signaling. These findings provide new insights into the procarcinogenic effects of tobacco smoke and may help to explain the increased rate of SPT in individuals who continue to smoke ( 25).
Materials. Keratinocyte basal and growth media were supplied by Clonetics Corp. DMEM was from Invitrogen Corp. AG1478 and PD98059 were acquired from Calbiochem. Human Matrigel matrix was from BD Biosciences. Transwell plates with 8-μm pore polycarbonate membrane inserts were purchased from Corning, Inc. [3H]glucosamine was purchased from DuPont/New England Nuclear. Amphiregulin and antiamphiregulin were from R&D Systems, Inc. Anti-EGFR antibody was purchased from Upstate. Antibodies to phosphorylated and unphosphorylated forms of ERK1/2 were from Cell Signaling Technology, Inc. Normal goat IgG and normal mouse IgG were obtained from Santa Cruz Biotechnology, Inc. Plasminogen activator assay substrate (d-Val-Leu-Lys-amino methyl coumarin) was obtained from MP Biomedicals. Human Glu-plasminogen, plasmin, α2 plasmin inhibitor, and antibodies to human uPA and plasmin were obtained from American Diagnostica, Inc. Amiloride and antisera to β-actin were obtained from Sigma Chemical Co. Human dermal fibroblasts were obtained from VEC Technologies, Inc.
Tissue culture. The MSK-Leuk1 cell line was established from a dysplastic leukoplakia lesion adjacent to a squamous cell carcinoma of the tongue ( 26). Cells were routinely maintained in keratinocyte growth medium supplemented with bovine pituitary extract. Cells were grown in basal medium for 24 h before treatment. Treatment with vehicle (PBS) or a saline extract of tobacco smoke (prepared as described below) was carried out under serum-free conditions. Cellular cytotoxicity was assessed by measurements of cell number, trypan blue exclusion, and release of lactate dehydrogenase. There was no evidence of cytotoxicity in any of our experiments.
Preparation of tobacco smoke. Cigarettes (2R4F, Kentucky Tobacco Research Institute) were smoked in a Borgwaldt piston-controlled apparatus (model RG-1) using the Federal Trade Commission standard protocol. The protocol variables attempt to mimic a standardized human smoking pattern (duration, 2 s/puff; frequency, 1 puff/min; volume, 35 mL/puff). Cigarettes were smoked one at a time in the apparatus and the smoke was drawn under sterile conditions into premeasured amounts of sterile PBS (pH 7.4). This smoke in PBS represents whole trapped mainstream smoke abbreviated as tobacco smoke ( 27). Quantitation of smoke content is expressed in puffs/mL of PBS with one cigarette yielding about 8 puffs drawn into a 5 mL volume. The final concentration of tobacco smoke in the cell culture medium is expressed as puffs/mL medium. Unless otherwise indicated, all treatments were carried out with either 0.015 or 0.03 puffs/mL tobacco smoke.
Preparation of [3H]glucosamine-labeled ECMs. The preparation of labeled ECM has been described previously ( 28). Human dermal fibroblasts were plated into 24-well plates (5 × 104 per well) in DMEM supplemented with 10% fetal bovine serum, penicillin (100 units/mL), streptomycin (100 μg/mL), and 4 mmol/L glutamine. On day 3, media were replaced with fresh media containing 1 μCi/well [3H]glucosamine. On day 6, the cell layer was removed by sequential exposure to 0.5% Triton X-100 in PBS (10 min) and 0.20 mmol/L NH4OH in PBS (3 min). Matrix-coated plates were washed thrice with sterile Dulbecco's PBS (DPBS) and allowed to dry in a laminar flow hood and then stored at 4°C.
ECM invasion assay. Invasion assays were carried out in a 24-well Transwell plates with 8.0-μm pore polycarbonate membrane inserts. Inserts were coated with Matrigel as follows: Matrigel was thawed on ice and diluted with ice-cold sterile water to 75 μg/mL. A 50-μL aliquot of Matrigel was rapidly spread over the surface of the prechilled inserts and allowed to air dry overnight. Before use, coated inserts were rehydrated with serum-free medium for 1 h. MSK-Leuk1 cells were harvested and resuspended to 2 × 105/mL basal medium. After 30 to 60 min of pretreatment with various inhibitors, tobacco smoke was added to the cell suspension. Treated cells (2 × 104 per insert) were added to the matrix-coated insert, and the insert was placed in a 24-well plate containing keratinocyte growth medium. After incubation at 37°C and 5% CO2 for 24 h, the membrane was fixed for 30 min in chilled 70% ethanol and stained for 25 min with 0.75% hematoxylin. Cells and ECM that were attached to the upper surface of the membrane were removed using a cotton swab. The membrane was then carefully removed from the insert and mounted onto a glass slide. The membranes were examined using a light microscope, and cells that migrated through the matrix-coated insert were counted.
Determination of plasminogen activator activity. MSK-Leuk1 cells were exposed to tobacco smoke and/or other treatments in serum-free medium as indicated in the figure legends. Conditioned media were collected into 1.5 mL microcentrifuge tubes and placed on ice before being cleared by centrifugation (5,000 rpm for 5 min at 4°C). Plasminogen activator activity was quantified using a sensitive functional assay for plasmin as described previously ( 29). Aliquots of conditioned medium were added to microtiter wells containing 82 μL DPBS plus 0.05% Tween 20, 13 μg of the plasmin substrate d-Val-Leu-Lys-amino methyl coumarin, and 0.5 μg bovine plasminogen. Samples were mixed and incubated at 37°C for 2.5 h. Cleavage of the substrate was monitored by measuring the increase in fluorescence in a Fluoroscan microplate reader (excitation: 330–380 nm; emission: 430–530 nm). Concentrations of uPA in the test samples were extrapolated from a standard curve prepared with high molecular weight uPA. Plasminogen activator activity in conditioned medium was completely inhibited when preincubated with a polyclonal antihuman uPA IgG.
Reverse transcription-PCR. RNA was prepared using RNeasy Mini kits from Qiagen. RNA (2 μg) was reversed transcribed using murine leukemia virus reverse transcriptase (Roche Applied Science) and oligo d(T)16 primer. The resulting cDNA was then used for amplification. The volume of the PCR was 25 μL and contained 5 μL cDNA, 50 mmol/L KCl, 10 mmol/L Tris-HCl (pH 8.3), 2 mmol/L MgCl2, 0.4 mmol/L deoxynucleotide triphosphates, 400 nmol/L forward primer, 400 nmol/L reverse primer, and 2.5 units Taq polymerase (Applied Biosystems). Samples were denatured at 95°C for 2 min and then amplified for 35 cycles in a thermocycler under the following conditions: 95°C for 30 s, 62°C for 30 s, and then 72°C for 45 s. Subsequently, extension was carried out at 72°C for 10 min. Human uPA primers were directed at 1181 to 1200 (forward, 5′-GTCACCACCAAAATGCTGTG-3′) and 1712 to 1693 (reverse, 5′-ATGCCCTGCCCTTTTTAACT-3′) of Genbank NM-002658. Primers for human β-actin have been described previously ( 30). PCR products were electrophoresed on a 1% agarose gel with 0.5 μg/mL ethidium bromide and photographed under UV light. The identity of each PCR product was confirmed by DNA sequencing. A computer densitometer (ChemDoc, Bio-Rad) was used to quantify the density of the different bands. Values are expressed in arbitrary units.
Statistics. Mean numbers of transmigrated cells, mean levels of uPA activity, or the mean percent of ECM degradation was compared using single- and two-factor ANOVA where appropriate. Individual comparisons between groups were made using the Newman-Keuls multiple comparison test. A difference between groups of P < 0.05 was considered significant.
Tobacco smoke stimulates cell invasiveness by inducing uPA. The effect of tobacco smoke on the ability of MSK-Leuk1 cells to transmigrate through a Matrigel-coated porous (8 μm) insert was determined. The addition of tobacco smoke to inserts led to a 2-fold increase in the number of cells that migrated through the ECM over 24 h ( Fig. 1 ). Given the reported role of uPA in cell migration, we investigated whether tobacco smoke induced uPA expression in MSK-Leuk1 cells. As shown in Fig. 2A , levels of uPA mRNA were markedly increased in cells treated with tobacco smoke for 6 to 12 h. Likewise, exposure to tobacco smoke led to a time-dependent increase in the levels of uPA activity in cellular conditioned medium ( Fig. 2B). We next determined whether tobacco smoke–induced uPA expression was responsible for the enhanced ability of these cells to traverse ECM-coated inserts ( Fig. 1). For this purpose, we used neutralizing anti-uPA IgG and amiloride, a selective inhibitor of uPA activity that has no effect on tissue type plasminogen activator or plasmin activities ( 31). As shown in Fig. 3A , the ability of cells to traverse the Matrigel-coated insert was markedly stimulated (2-fold) by exposure to tobacco smoke. The enhanced migration was completely blocked by the addition of anti-uPA IgG, whereas normal IgG had no effect. Likewise, preincubation of cells with amiloride blocked tobacco smoke–induced invasion ( Fig. 3A). Thus, enhanced uPA expression is causally linked to tobacco smoke–induced migration of MSK-Leuk1 cells through ECM.
Tobacco smoke stimulates the invasion of MSK-Leuk1 cells. Cells (2 × 104) were aliquoted into an insert containing a porous (8 μm) polycarbonate Matrigel-coated membrane. The cells in the insert were then treated with 0 to 0.03 puffs/mL tobacco smoke in basal medium. The insert was placed into a well containing growth medium and incubated at 37°C for 24 h. Cells that migrated into the lower well were counted after being fixed and stained. Columns, mean (n = 3); bars, SD. *, P < 0.05, compared with vehicle-treated control. These data are representative of three independent experiments.
Tobacco smoke stimulates the expression and release of uPA. Cells were treated with vehicle (C) or tobacco smoke (TS) for 3, 6, or 12 h. A, reverse transcription-PCR (RT-PCR) was used to determine the amounts of mRNAs for uPA and β-actin. B, amount of uPA activity was measured in medium from vehicle-treated or tobacco smoke–treated cells. Columns, mean (n = 3); bars, SD. *, P < 0.05, tobacco smoke compared with control.
uPA is critical for tobacco smoke–mediated degradation of ECM and increased cell invasion. A to C, cells were suspended in basal medium and incubated for 1 h with the indicated treatments [antibodies to uPA or IgG at 10 μg/mL, 50 μmol/L amiloride (Am), plasminogen inhibitor (PI) at 5 μg/mL]. Cells (2 × 104) were then aliquoted into a Matrigel-coated insert. The cells in the insert were then treated with vehicle or tobacco smoke. The insert was placed into a well containing growth medium and incubated at 37°C for 24 h. A and C, cells that migrated into the lower well were counted after being fixed and stained. B, medium was collected and plasmin concentration was determined. Columns, means (n = 4); bars, SD. *, P < 0.05, compared with tobacco smoke. D, cells were plated on insoluble [3H]glucosamine-labeled ECM in basal medium. Following adherence, medium was replaced with either control or tobacco smoke–conditioned medium. Treatments with 0.5 μg/mL plasminogen (Plg) or 50 μmol/L amiloride were as indicated. Twenty-four hours later, incubation media were recovered and solubilized [3H] activity was determined as described in Materials and Methods. Columns, mean (n = 4); bars, SD. *, P < 0.05, tobacco smoke compared with untreated control and tobacco smoke + plasminogen + amiloride compared with tobacco smoke + plasminogen.
Plasminogen activation and subsequent degradation of ECM components is thought to be a principal mechanism by which enhanced uPA expression stimulates cellular invasion. To test whether tobacco smoke–induced uPA expression led to plasminogen activation in the Transwell culture system, 24-h conditioned media were collected from the inserts and assayed for plasmin activity. In these studies, cellular incubation medium was not supplemented with exogenous plasminogen. However, Matrigel contains variable amounts of plasminogen ( 32). As shown in Fig. 3B, medium derived from control cells cultured on Matrigel contained low levels of plasmin activity. The level of plasmin activity in the conditioned medium increased dramatically when cells were exposed to tobacco smoke. Furthermore, the tobacco smoke–induced increase in plasmin activity was inhibited by anti-uPA IgG or amiloride. To determine whether tobacco smoke–induced uPA-dependent plasmin activity was necessary for increased cell migration through ECM, migration was monitored in the presence of excess α2 plasmin inhibitor. As shown in Fig. 3C, the addition of α2 plasmin inhibitor to cells blocked their migration through Matrigel in response to tobacco smoke.
uPA-dependent plasminogen activation plays an important role in cellular migration via plasmin cleavage of ECM components. Hence, it was next important to determine the effect of tobacco smoke on ECM degradation by MSK-Leuk1 cells. Cell-derived matrices, metabolically labeled with [3H]glucosamine, are useful as a tracer substrate because [3H]glucosamine is incorporated into proteoglycans and adhesive glycoproteins that are susceptible to plasmin cleavage. When cells were plated on labeled matrices in medium alone, a small amount of [3H] activity was solubilized ( Fig. 3D). The addition of exogenous plasminogen, the substrate for uPA, led to ∼2-fold increase in solubilization of labeled ECM, an effect that was blocked by the uPA inhibitor amiloride. Exposure of cells to tobacco smoke alone led to approximately a doubling of ECM degradation. When cells were incubated with tobacco smoke and plasminogen, ECM degradation was dramatically increased (5-fold), an effect that was blocked by the addition of amiloride ( Fig. 3D). Taken together, these data indicate that tobacco smoke–mediated induction of uPA leads to increased plasmin production, resulting, in turn, in increased ECM degradation and enhanced ability of MSK-Leuk1 cells to migrate through ECM.
EGFR signaling is responsible for tobacco smoke–mediated induction of uPA and invasiveness. We next investigated the signaling pathway by which tobacco smoke induced uPA and cell invasiveness. Activation of EGFR signaling can induce uPA expression ( 33). Previously, we found that tobacco smoke stimulated the synthesis and release of amphiregulin, resulting in activation of EGFR signaling ( 27). It was logical, therefore, to investigate whether tobacco smoke induced uPA expression by an EGFR-dependent mechanism. As shown in Fig. 4A and B , tobacco smoke–mediated induction of uPA was suppressed by treatment with either a neutralizing antibody to EGFR or AG1478, an inhibitor of EGFR tyrosine kinase. Importantly, the inductive effect of tobacco smoke was also suppressed by the addition of an antibody to amphiregulin. In contrast, control IgG had no effect on the induction of uPA by tobacco smoke. To confirm the significance of amphiregulin as an inducer of uPA, exogenous amphiregulin was used. Treatment with amphiregulin led to dose-dependent induction of uPA ( Fig. 4C). We next determined whether tobacco smoke–induced transmigration through Matrigel-coated inserts was EGFR dependent. For this purpose, cells were preincubated with AG1478 or neutralizing antibodies to EGFR or amphiregulin. As seen in Fig. 4D, tobacco smoke–induced transmigration was blocked by AG1478 or antibodies to EGFR or amphiregulin.
Tobacco smoke–mediated induction of uPA is EGFR dependent. Cells were grown in basal medium for 24 h. A and B, cells then received the indicated treatments [antibodies to EGFR, amphiregulin (AR), or IgG at 10 μg/mL; 250 or 500 nmol/L AG1478] for 2 h before being exposed to tobacco smoke for 6 h. A, RT-PCR was used to determine the amount of mRNAs for uPA and β-actin. Results of the data shown are expressed in arbitrary units (A.U.). B, amount of uPA activity was measured in medium. Columns, mean (n = 3); bars, SD. *, P < 0.05, compared with tobacco smoke. C, cells were treated with 0 to 20 ng/mL of amphiregulin for 6 h. RT-PCR was used to determine the amounts of mRNAs for uPA and β-actin. D, cells were suspended in basal medium and incubated for 1 h with the indicated treatments (antibodies to EGFR, amphiregulin, or IgG at 10 μg/mL; 500 nmol/L AG1478). Cells (2 × 104) were then aliquoted into an insert containing a porous (8 μm) polycarbonate Matrigel-coated insert. The cells in the insert were then treated with vehicle or tobacco smoke. The insert was placed into a well containing growth medium and incubated at 37°C for 24 h. Cells that migrated into the lower well were then counted after being fixed and stained. Columns, mean (n = 4); bars, SD. *, P < 0.05, compared with tobacco smoke.
Stimulation of EGFR signaling leads to activation of ERK1/2 MAPK. It was of interest, therefore, to determine whether ERK1/2 was involved in tobacco smoke–mediated induction of uPA and cellular transmigration. As shown in Fig. 5A , tobacco smoke caused a rapid increase in ERK1/2 activity. Notably, PD98059, an inhibitor of MAPK kinase, suppressed tobacco smoke–mediated induction of uPA expression and activity ( Fig. 5B) and the migration of MSK-Leuk1 cells through ECM ( Fig. 5C).
ERK1/2 is critical for tobacco smoke–mediated induction of cell invasion. A, cells were treated with tobacco smoke for 0 to 120 min. Cellular protein (100 μg/lane) was loaded onto a 10% SDS-polyacrylamide gel, electrophoresed, and subsequently transferred onto nitrocellulose. The blot was probed with antibodies to the phosphorylated and unphosphorylated forms of ERK1/2. Results of the data shown are expressed in arbitrary units. B, cells were treated with vehicle or PD98059 for 2 h. Subsequently, the cells received either vehicle or tobacco smoke as indicated for 6 h. Left, RT-PCR was used to determine the amounts of mRNAs for uPA and β-actin. Results of the data shown are expressed in arbitrary units. Right, the amount of secreted uPA was measured in the medium. Columns, mean (n = 3); bars, SD. *, P < 0.05, compared with tobacco smoke. C, cells were suspended in basal medium and incubated for 1 h with vehicle or 25 μmol/L PD98059. Cells (2 × 104) were then aliquoted into an insert containing a porous (8 μm) polycarbonate Matrigel-coated insert. The cells in the insert were then treated with vehicle or tobacco smoke. The insert was placed into a well containing growth medium and incubated at 37°C for 24 h. Cells that migrated into the lower well were then counted after being fixed and stained. Columns, mean (n = 3); bars, SD. *, P < 0.05, compared with tobacco smoke.
The mechanisms responsible for clonal spreading of noninvasive leukoplakic lesions are unknown ( 3, 4). Several lines of evidence suggest that uPA, together with its high-affinity receptor, uPAR, is important in initiating a proteolytic cascade that stimulates cell migration ( 7– 12). In this regard, protease activities expressed by buccal cells obtained from smokers and leukoplakia patients were significantly elevated when compared with a nonsmoking control group ( 34). In experiments reported here, we have extended these observations by showing that exposure to tobacco smoke led to urokinase-dependent plasminogen activation and increased cell migration of MSK-Leuk1 cells. The importance of uPA in mediating cell invasion was supported by evidence that antibodies to uPA or treatment with amiloride, an inhibitor of uPA, blocked tobacco smoke–mediated induction of cell invasion. The induction of uPA by tobacco smoke stimulated the conversion of plasminogen to plasmin, resulting, in turn, in the degradation of ECM and cell invasion. This mechanism may help to explain why some clinically determined SPT have a common clonal origin in smokers ( 3, 4). Consistent with this notion, patients who continue to smoke after the successful treatment of their index head and neck malignancy have a significantly increased risk of developing SPT ( 25). Of course, SPT may also be a consequence of field cancerization ( 4, 6). Notably, the discovery that tobacco smoke stimulated cell invasion raises the intriguing possibility that clonal migration may occur as a consequence of environmental factors in addition to properties that are intrinsic to the neoplastic cell. Although there is extensive evidence that oncogenes induce uPA and cell invasion ( 7, 35), this study suggests that tobacco smoke contains chemicals that can mimic these effects of oncogenes. To our knowledge, this is the first study to highlight the potential role of a reversible exogenous factor (i.e., tobacco smoke) in driving cell invasion. Numerous lines of investigation suggest that the uPA-uPAR axis plays a significant role in metastasis ( 12, 23, 24, 37). Based on the findings in this study, we speculate that tobacco smoke–mediated activation of the uPA-uPAR axis may contribute to the worse prognosis of cancer patients who continue to smoke.
Several observations support a critical role for the EGFR in tobacco smoke–mediated induction of uPA and cell invasiveness. Previously, we showed that tobacco smoke stimulated amphiregulin transcription, resulting in activation of EGFR signaling ( 30). Here, we found that AG1478, an EGFR tyrosine kinase inhibitor, or antibodies to the ligand-binding site of EGFR or amphiregulin blocked tobacco smoke–mediated induction of uPA and cell invasion. Moreover, treatment of cells with exogenous amphiregulin led to marked induction of uPA. These findings add to growing evidence that disrupting the release or actions of amphiregulin may inhibit carcinogenesis ( 37, 38). Although this is the first study to show that tobacco smoke induced uPA by an EGFR-dependent mechanism, activation of EGFR is known to regulate the expression of uPA in other systems ( 33). Previously, growth factor–mediated activation of EGFR was found to stimulate ERK1/2 activity, leading, in turn, to increased uPA expression ( 33, 39). Similarly, in the current study, several findings suggest an important role for ERK1/2 in tobacco smoke–mediated induction of uPA. Treatment with tobacco smoke activated ERK1/2 MAPK. More importantly, PD98059, an inhibitor of MAPK kinase, blocked tobacco smoke–mediated induction of uPA expression and activity and the migration of MSK-Leuk1 cells through ECM. The activator protein-1 transcription factor complex is likely to contribute to the induction of uPA because it can regulate uPA transcription ( 40) and is activated by ERK1/2. Taking these data together, we conclude that tobacco smoke–mediated activation of EGFR→ERK1/2 MAPK led to induction of uPA and increased cell migration. Previously, binding of uPA to uPAR was reported to stimulate EGFR→ERK1/2 MAPK signaling ( 41). Hence, it is possible that tobacco smoke will stimulate a positive feedback loop whereby activation of the EGFR→ERK1/2 MAPK pathway causes induction of uPA, which binds to uPAR, causing further activation of EGFR signaling and induction of uPA. Clearly, this type of positive feedback loop could amplify the procarcinogenic effects of tobacco smoke. Inhibitors of EGFR tyrosine kinase are clinically available. This study strengthens the rationale for evaluating whether an inhibitor of EGFR tyrosine kinase can prevent or delay the development of tobacco smoke–related SPT of the aerodigestive tract.
Grant support: NIH grants R01 CA82578 and R01 HL073375 and Center for Cancer Prevention Research.
Sidransky D, Frost P, Von Eschenbach A, Oyasu R, Preisinger AC, Vogelstein B. Clonal origin of bladder cancer. N Engl J Med 1992; 326: 737–40.
Hafner C, Knuechel R, Stoehr R, Hartmann A. Clonality of multifocal urothelial carcinomas: 10 years of molecular genetic studies. Int J Cancer 2002; 101: 1–6.
Jang SJ, Chiba I, Hirai A, Hong WK, Mao L. Multiple oral squamous epithelial lesions: are they genetically related? Oncogene 2001; 20: 2235–42.
Mao L, Hong WK, Papadimitrakopoulou V. Focus on head and neck cancer. Cancer Cell 2004; 5: 311–6.
Franklin WA, Gazdar AF, Haney J, et al. Widely dispersed p53 mutation in respiratory epithelium. J Clin Invest 1997; 100: 2133–7.
Slaughter DP, Southwick HW, Smejkal W. Field cancerization in oral stratified squamous epithelium: clinical implications of multicentric origin. Cancer 1953; 6: 963–8.
Aguirre Ghiso JA, Alonso DF, Farias EF, Gomez DE, Bal de Kier Joffe E. Deregulation of signaling pathways controlling urokinase production: its relationship with invasive phenotype. Eur J Biochem 1999; 263: 295–304.
Estreicher A, Muhlhauser J, Carpentier JL, Orci L, Vassalli JD. The receptor for urokinase type plasminogen activator polarizes expression of the protease to the leading edge of migrating monocytes and promotes degradation of enzyme inhibitor complexes. J Cell Biol 1990; 111: 783–92.
Ploplis VA, French EL, Carmeliet P, Collen D, Plow EF. Plasminogen deficiency differentially affects recruitment of inflammatory cell populations in mice. Blood 1998; 91: 2005–9.
Kindzelskii AL, Amhad I, Keller D, et al. Pericellular proteolysis by leukocytes and tumor cells on substrates: focal activation and the role of urokinase-type plasminogen activator. Histochem Cell Biol 2004; 121: 299–310.
Festuccia C, Dolo V, Guerra F, et al. Plasminogen activator system modulates invasive capacity and proliferation in prostatic tumor cells. Clin Exp Metastasis 1998; 16: 513–28.
Pulukuri SM, Gondi CS, Lakka SS, et al. RNA interference-directed knockdown of urokinase plasminogen activator and urokinase plasminogen activator receptor inhibits prostate cancer cell invasion, survival, and tumorigenicity in vivo. J Biol Chem 2005; 280: 36529–40.
Henkin J, Marcotte P, Yang HC. The plasminogen-plasmin system. Prog Cardiovasc Dis 1991; 34: 135–64.
Kirchheimer JC, Remold HG. Functional characteristics of receptor-bound urokinase on human monocytes: catalytic efficiency and susceptibility to inactivation by plasminogen activator inhibitors. Blood 1989; 74: 1396–402.
Ellis V, Wun TC, Behrendt N, Ronne E, Dano K. Inhibition of receptor-bound urokinase by plasminogen-activator inhibitors. J Biol Chem 1990; 265: 9904–8.
Moser TL, Enghild JJ, Pizzo SV, Stack MS. The extracellular matrix proteins laminin and fibronectin contain binding domains for human plasminogen and tissue plasminogen activator. J Biol Chem 1998; 268: 18917–23.
Richardson M, Hatton MW, Moore S. The plasma proteases, thrombin and plasmin, degrade the proteoglycan of rabbit aorta segments in vitro: an integrated ultrastructural and biochemical study. Clin Invest Med 1988; 11: 139–50.
Kost C, Benner K, Stockmann A, Linder D, Preissner KT. Limited plasmin proteolysis of vitronectin. Characterization of the adhesion protein as morpho-regulatory and angiostatin-binding factor. Eur J Biochem 1996; 236: 682–8.
Visse R, Nagase H. Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry. Circ Res 2003; 92: 827–39.
Gyetko MR, Sud S, Chen GH, Fuller JA, Chensue SW, Toews GB. Urokinase-type plasminogen activator is required for the generation of a type 1 immune response to pulmonary Cryptococcus neoformans infection. J Immun 2002; 168: 801–9.
Sitrin RG, Shollenberger SB, Strieter RM, Gyetko MR. Endogenously produced urokinase amplifies tumor necrosis factor-α secretion by THP-1 mononuclear phagocytes. J Leukoc Biol 1996; 59: 302–11.
Legrand C, Polette M, Tournier JM, et al. uPA/plasmin system-mediated MMP-9 activation is implicated in bronchial epithelial cell migration. Exp Cell Res 2001; 264: 326–36.
Andreasen PA, Kjøller L, Christensen L, Duffy MJ. The urokinase-type plasminogen activator system in cancer metastasis: a review. Int J Cancer 1997; 72: 1–22.
Crowley CW, Cohen RL, Lucas BK, Liu G, Shuman MA, Levinson AD. Prevention of metastasis by inhibition of the urokinase receptor. Cell Biol 1993; 90: 5021–5.
Khuri FR, Lee JJ, Lippman SM, et al. Randomized phase III trial of low-dose isotretinoin for prevention of second primary tumors in stage I and II head and neck cancer patients. J Nat Cancer Inst 2006; 98: 441–50.
Sacks PG. Cell, tissue and organ culture as in vitro models to study the biology of squamous cell carcinomas of the head and neck. Cancer Metastasis Rev 1996; 15: 27–51.
Moraitis D, Du B, De Lorenzo MS, et al. Levels of cyclooxygenase-2 are increased in the oral mucosa of smokers: evidence for the role of epidermal growth factor receptor and its ligands. Cancer Res 2005; 65: 664–70.
Falcone DJ, Borth W, Khan KMF, Hajjar KA. Plasminogen-mediated matrix invasion and degradation by macrophages is dependent on surface expression of annexin II. Blood 2001; 97: 777–84.
Falcone DJ, McCaffrey TA, Haimovitz-Friedman A, Garcia M. Transforming growth factor-β1 stimulates macrophage urokinase expression and release of matrix-bound basic fibroblast growth factor. J Cell Physiol 1993; 155: 595–605.
Du B, Altorki NK, Kopelovich L, Subbaramaiah K, Dannenberg AJ. Tobacco smoke stimulates the transcription of amphiregulin in human oral epithelial cells: evidence of a cyclic AMP-responsive element binding protein-dependent mechanism. Cancer Res 2005; 65: 5982–8.
Vassalli J-D, Belin D. Amiloride selectively inhibits the urokinase-type plasminogen activator. FEBS Let 1987; 214: 187–91.
Farina AR, Tiberio A, Tacconelli A, Cappabianca L, Gulino A, Mackay AR. Identification of plasminogen in Matrigel and its activation by reconstitution of this basement membrane extract. Biotechniques 1996; 21: 904–9.
Mahabeleshwar GH, Das R, Kundu GC. Tyrosine kinase, p56lck-induced cell motility, and urokinase-type plasminogen activator secretion involve activation of epidermal growth factor receptor/extracellular signal regulated kinase pathways. J Biol Chem 2004; 279: 9733–42.
Manzone H, Billings PC, Cummings WN, et al. Levels of proteolytic activities as intermediate marker endpoints in oral carcinogenesis. Cancer Epidemiol Biomarkers Prev 1995; 4: 521–7.
Urban P, Vuaroqueaux V, Labuhn M, et al. Increased expression of urokinase-type plasminogen activator mRNA determines adverse prognosis in ErbB2-positive primary breast cancer. J Clin Oncol 2006; 24: 4245–53.
Rao JS, Gondi C, Chetty C, Chittivelu S, Joseph PA, Lakka SS. Inhibition of invasion, angiogenesis, tumor growth, and metastasis by adenovirus-mediated transfer of antisense uPAR and MMP-9 in non-small cell lung cancer cells. Mol Cancer Ther 2005; 4: 1399–408.
Willmarth NE, Ethier SP. Autocrine and juxtacrine effects of amphiregulin on the proliferative, invasive, and migratory properties of normal and neoplastic human mammary epithelial cells. J Biol Chem 2006; 281: 37728–37.
Castillo J, Erroba E, Perugorria MJ, et al. Amphiregulin contributes to the transformed phenotype of human hepatocellular carcinoma cells. Cancer Res 2006; 66: 6129–38.
Simon C, Juarez J, Nicolson GL, Boyd D. Effect of PD 098059, a specific inhibitor of mitogen-activated protein kinase kinase, on urokinase expression and in vitro invasion. Cancer Res 1996; 56: 5369–74.
DeCesare D, Vallone D, Caracciolo A, Sassone-Corsi P, Nerlov C, Verde P. Heterodimerization of c-Jun with ATF-2 and c-Fos is required for positive and negative regulation of the human urokinase enhancer. Oncogene 1995; 11: 365–76.
Jo M, Thomas KS, O'Donnell DM, Gonias SL. Epidermal growth factor receptor-dependent and -independent cell-signalling pathways originating from the urokinase receptor. J Biol Chem 2003; 278: 1642–6.
You are going to email the following Tobacco Smoke Induces Urokinase-Type Plasminogen Activator and Cell Invasiveness: Evidence for an Epidermal Growth Factor Receptor–Dependent Mechanism
Cancer Res September 15 2007 (67) (18) 8966-8972; DOI: 10.1158/0008-5472.CAN-07-1388
Abstract OT2-09-02: A phase I dose escalation study of topical bexarotene in women at high risk for breast cancer
Abstract OT2-09-01: Pilot study of denosumab in BRCA1/2 mutation carriers scheduling for risk-reducing salpingo-oophorectomy
Abstract OT3-01-02: Randomized controlled trial of web-based decision support tools for high-risk women and primary care providers to increase breast cancer chemoprevention
Show more Prevention


Learn how to locate schools with training programs in French cooking. Find out what courses are included in degree and certificate programs, including externships and online options. Schools offering Art of Cooking degrees can also be found in these popular choices.
Interested students can select from associate's and bachelor's degrees in culinary arts. These programs we've listed have French cooking classes.
How Do I Find a French Cooking School?
There are non-accredited, private, for-profit institutions that advertise themselves as French cooking schools. Though some of their courses or programs may satisfy you, a little investigating might be advisable before you invest your time and money. There are a couple of good sources you can use to locate accredited, reliable institutions that offer training in French cuisine.
One of the features of the National Center for Education Statistics (NCES) website is an online, searchable database of postsecondary education institutions. A search yields nearly 500 schools that offer certificate or degree programs in culinary arts, chef training, cooking or related services. French cooking technique or French cuisine classes may be available in a school's culinary arts or hospitality department.
The American Culinary Federation, Inc. (ACF) is a professional organization for chefs and cooks. The Education Foundation Accrediting Commission of the ACF is recognized by the Council for Higher Education Accreditation. On its website, the ACF maintains a list of accredited schools offering certificates, diplomas and degrees dealing with culinary arts.
Online French cooking lessons are rare. You may be able to learn about French cooking online through private, for-profit organizations, schools that aren't accredited or websites not affiliated with a school. Often these programs are delivered as tutorials or videos. Some information is also available by way of online French cooking magazines or recipe books. These are all generally intended as personal-development courses and don't carry any academic credits.
What Are Some Available Programs?
Depending on the school, it can take you 20-24 months to complete a 60-99 credit program leading to an associate's degree in culinary arts. Often, schools require you to complete the associate's degree program in order to be admitted to their bachelor's degree program.
Bachelor's degree programs vary from 124-199 credits and can take 38-48 months to complete. Typical French cooking-related courses common to each program can include Mediterranean cuisine, classical French cuisine, international cuisine and international pastry. Bachelor's degree programs may also include French language studies.
Both degree programs often entail an externship at a school-approved food service operation. Externships might be paid positions and can last as long as 18 weeks. Depending on a school's affiliations, you may have the opportunity to serve your externship in France.
Which Schools Offer Associate's Degrees in French Cooking?
Make sure that your degree program includes coursework in French cooking. Consider these schools to get started in your search.
Which Schools Offer Bachelor's Degrees in French Cooking?
Consider these 4-year programs to earn your bachelor's degree in culinary arts. Courses in French cuisine through these degrees are available.
Are There Any Reputable Not-For-Credit Programs?
There are accredited for-profit and not-for-profit schools offering programs that can take you up to a year to complete. These lead to specialized certificates or school-granted diplomas in different aspects of French cooking. These awards often carry no academic credit and aren't transferable to a degree program, but are meant to enhance your employment or advancement prospects. You can often find such schools through the NCES or ACF.
You can study French cooking through various undergraduate programs. Plenty of options exist for a degree in culinary arts with classes in French cooking.


Jacob Dean was a wonderful Maker with which to work. He was both competent and knowledgeable. He was more than patient regarding the timeline associated with a municipal job and best of all, he had a great attitude throughout our journey.
Thank you Jacob. We appreciate your thoughtfulness and effort in the creation of our sculpture.
This piece is a public commission for the city of Coconut Creek Florida (aka) The Butterfly Capital of the World.
Their interest in a large, rustic butterfly piece was posted here on Custommade.com. After some deliberation and design, we chose to create a Giant Swallowtail butterfly, after the Art Nouveau style, contour lined wings and solid sculpted body.
The Butterfly is all fabricated steel, mostly recycled, but includes stock sections of Corten steel to preserve it from rust and decay. It stands 13 ft tall.


Goldcar, a market leading company in holiday vehicle rental, collaborates with the town of San Juan in its reforestation plan for the area with the aim of generating a positive impact on the community and contributing to Promote environmental education amongst its employees.
During the day yesterday, around 25 employees of Goldcar's central services participated in a reforestation project to plant 120 shrubs of native species such as carob, carob, wild olive, lavender, rosemary and albaida, amongst others. . All of them were acquired in the San Juan nursery with the aim of promoting local trade.
For the development of the project, the employees have had the support of a Red Cross team that has been in charge of guiding them during the planting of the trees. Thanks to them, it has been possible to answer such questions as the type of soil on which they is being planted, why specific plants have been chosen or, for example, what will be the repercussion of this action.
The day was also attended by the director of Human Resources of Goldcar, Tonica Safont, the mayor of the municipality of San Juan, Jaime Albero, and the technician for the Environment, Darío Moreno i Alzuyet, who collaborated with Goldcar employees with the reforestation.
Goldcar's participation in this reforestation plan of the town of San Juan is another example of the company's commitment to protecting the environment. In fact, Goldcar has established a number of measures, included in its Corporate Social Responsibility Report, aimed at rationalising energy consumption and minimising its carbon footprint.
Among the most noteworthy initiatives launched by Goldcar to minimise its carbon footprint is the incorporation of 255 hybrid, LPG and electric vehicles into its fleet. In addition, the company continues to strengthen its Goldcar Blue program, an electric car hire service available in Palma, Madrid and Barcelona, which aims to promote sustainable mobility among its customers. These measures have contributed to the reduction by more than 4% of CO2 emissions per kilometre travelled by the Goldcar rental fleet.


This page is about WordPerfect macros that can be used for converting WordPerfect files into Word, RTF, or PDF format. The descriptions on this page refer to WPDOS running natively (without vDosWP or DOSBoxWP) under 32-bit Windows.
Very similar macros are installed when you install the vDosWP and DOSBoxWP systems, and if you use either of those systems, see the description of the corresponding macros provided on the pages on this site that describe those systems. If you use either of those systems, you do not need to look at this page, and you should not download anything from this page! Use the macros that are installed when you installed those other systems!
These macros use Windows scripts that may be used separately, without requiring or using WPDOS. See a separate page for details.
See also a separate page for standalone programs that convert WP files into Word or PDF files under any Windows version.
See also the note on a separate page about WPDOS files that contain the euro symbol. See a separate page for information on importing Microsoft Word files into WordPerfect for DOS.
For other methods of creating PDF files directly from WPDOS, see a separate page about "printing" PDF files from WPDOS. The methods on that page will produce more accurate results than the methods described on the page you are reading now, because the methods on the other page "print" a PDF file directly from WordPerfect instead of using Microsoft Word or LibreOffice to convert the file first.
All other methods described on this page require either Word or LibreOffice to be installed on your system. These are the requirements for the Microsoft Word-based macros and the LibreOffice-based macros. Read these requirements carefully!
LibreOffice: The script and macros should work with LibreOffice versions 3.4 or later.
Note: These macro systems are frequently updated. If you find that the latest version of Microsoft Word or LibreOffice causes your script to stop working, please replace the script with the current version.
Note: If, when opening a document converted by one of these macros, Word repeatedly displays the error message "Word cannot start the converter mswrd632.wpc" or "Cannot load Word for Windows 6.0 files", please consult this Microsoft information page. This problem is caused entirely by a security update installed by Microsoft starting in 2009; it is not caused by these scripts!
Warning: The WP macros described will work only when used with WPDOS running natively (in a "DOS Window") under 32-bit Windows. They will not work correctly with vDosWP or DOSBoxWP! If you use the vDosWP or DOSBoxWP systems, use the similarly-named macros that are installed with those systems!
Using a copy of Microsoft Word for Windows already installed on your computer, a WPDOS macro automatically exports the document open in WPDOS to Word or PDF format, with options to correct Word's choice of fonts to apply to the converted document, and with options to make other minor changes in Word's formatting. (This macro method works with Word 2002, 2003, 2007, 2010, and later versions; PDF conversion requires Word 2007 SP2, 2010, or later.) This macro launches a separate (supplied) Windows script program.
Remember that your original WPDOS files are not changed in this process and remain on your disk with their original names!
Further details are provided in the separate sections below.
If (1) you use a Macintosh computer, and (2) you have WordPerfect for DOS files or WordPerfect for Windows files that you want to open in Microsoft Word for the Mac, see the general page on WPDOS files imported into Word.
Important warning: This macro is intended for use with WPDOS running natively (in a "DOS Window") under 32-bit Windows. It will not work correctly if used with vDosWP or DOSBoxWP! If you use the vDosWP or DOSBoxWP systems, use the similarly-named macro that is installed with those systems!
Second important warning: This macro may cause WPDOS to lock up under 32-bit Windows 7. Be careful to save your files before using the macro.
This system uses a WPDOS 5.1 macro to launch a Windows script that uses Microsoft Word to convert the WP document currently on screen into Word or PDF format. The macro requires the script, but the script can also be used as a standalone program. You must have Microsoft Word installed on your system.
In WPDOS, use Shift-F1, 6 - Location of Files to find your Keyboard/Macro Files directory.
Download the WP5WordConv.zip archive file. Extract the WORDCONV.WPM and place it in the Keyboard/Macro Files directory. Extract the WP2MSW.VBS file and place it in the root folder of the drive that contains WPDOS; if WPDOS is in C:\WP51, then place the file in C:\; if WPDOS is in in E:\WP51, then place the file in E:\.
Press F7 to close the macro.
Open a WordPerfect file in WPDOS. Press Alt-F10, WORDCONV, and follow the prompts. A Word-format file will be created with the same name as the current WPDOS file, but with a new .DOC extension added to the existing name.
Press F7 to close the macro editor.
For instructions on modifying the script so it corrects Word's choice of fonts in the exported files, open the WP2MSW.VBS script in Windows Notepad or a similar text editor, and modify the script as explained in the instructions included in the script itself.
For instructions on using the WP2MSW.VBS script as a separate Windows application (not launched from a WP macro), see a description on another page.
This system uses a WPDOS 6.x macro to launch a Windows script that uses Microsoft Word to convert the WP document currently on screen into Word or PDF format. The macro requires the script, but the script can also be used as a standalone program. You must have Microsoft Word installed on your system.
In WPDOS, use Shift-F1, 5 - Location of Files, then Macro/Keyboard/Button Bar, and 1 - Personal Path, to find your personal macro directory.
Download the WP6WordConv.zip archive file. Extract the WORDCONV.WPM and the WP2MSW.VBS file and place both files in your personal macro directory.
To use the macro, open a WordPerfect file in WPDOS. Press Alt-F10, then enter WORDCONV and follow the prompts. A Word-format file will be created with the same name as the current WPDOS file, but with a new .DOC extension added to the existing name.
PDF, Long Filename, and other options. If you want to use the macro to create PDF output (Word 2007 SP2 or later required), or if you want the option to specify the name of the exported file, or if you want to use the option that uses the Document Descriptive Summary (Long Name) as the output filename, then press Ctrl-F10, enter WORDCONV, and choose Edit. This will open the macro file in the editing screen and you can set the options described in the macro itself.
Download the WP5LibrConv.zip archive file. Extract the LIBRCONV.WPM and place it in the Keyboard/Macro Files directory. Extract the WP-LO.VBS file and place it in the root folder of the drive that contains WPDOS; if WPDOS is in C:\WP51, then place the file in C:\; if WPDOS is in in E:\WP51, then place the file in E:\.
Open a WordPerfect file in WPDOS. Press Alt-F10, LIBRCONV, and follow the prompts. A Word-format file will be created with the same name as the current WPDOS file, but with a new .DOC extension added to the existing name.
For instructions on using the WP-LO.VBS script as a separate Windows application (not launched from a WP macro), see a description on another page.
Download the WP6LibrConv.zip archive file. Extract the LIBRCONV.WPM and the WP-LO.VBS file and place both files in your personal macro directory.
To use the macro, open a WordPerfect file in WPDOS. Press Alt-F10, then enter LIBRCONV and follow the prompts. A Word-format file will be created with the same name as the current WPDOS file, but with a new .DOC extension added to the existing name.
PDF, Long Filename, and other options. If you want to use the macro to create PDF output (Word 2007 SP2 or later required), or if you want the option to specify the name of the exported file, or if you want to use the option that uses the Document Descriptive Summary (Long Name) as the output filename, then press Ctrl-F10, enter LIBRCONV, and choose Edit. This will open the macro file in the editing screen and you can set the options described in the macro itself.
Q. I was stupid enough to download and use your macros and scripts, and the results aren't as good as I wanted. You have destroyed my files! The fonts are all wrong! The formatting is wrong! Everything is a total disaster! Word uses fonts with weird names like Shruti or Uighur instead of the fonts I carefully chose in WordPerfect! I lost all the work I did over the last fifteen years! This is all your fault!
A. Breathe deeply, make an effort to stay calm, and read the following sentences very slowly until you are absolutely sure that you understand them - and I mean really understand them. First, your original WordPerfect files have not been changed at all. They are still on your disk, exactly where they have always been, with exactly the same content and format that they have always had, and exactly the same names. You are complaining about the mistakes that Microsoft Word, and only Microsoft Word, made when creating copies of your original files in a different format. Remember, it was Microsoft Word and only Microsoft Word that decided which fonts to use in the exported files that it created! My script includes features that let you fix the problems caused by Word, by specifying in the script the fonts that Word should use when converting your file. But you will need to calm yourself and read the instructions in the script file before you can use these features. Also, please complain to Microsoft about the bugs and limitations of its file converters. It does you no good to complain to me.
Q. You said I could use your macro to convert WP files to PDF format using Microsoft Word, but when I do, a message pops up in Windows saying that I can't do that! I want my money back!
A. First, I don't think you paid me any money, so I can't pay it back. Next, did you read the clear and carefully spelled-out instructions that explain that you must have Word 2007 SP2 or later if you want to use these methods to create PDF files? This page (the page you are reading now) explains that crucial point many, many times. You presumably have Word 2000, Word 2002, Word 2003, or a copy of Word 2007 that you have not updated to SP2 - although, if you have Word 2007, Windows can update Word 2007 automatically for you so that you can create PDF files.


Based on their acclaimed best-selling book of the same name, Jean Jacques Machado and Jay Zeballos' highly anticipated three-DVD set, The Grappler's Handbook: Gi and No-Gi Techniques, serves as a martial arts multimedia companion wherein the two Brazilian jiu-jitsu masters demonstrate takedowns, chokes, holds and submissions in living color and in exhaustive detail. Filmed at the Jean Jacques Machado Academy in Los Angeles, this set will offer multi-angle coverage (front, three-quarters and overhead) of each technique with step-by-step instructions, contextual explanations for each technique's application, and an optional on-screen subtitle track with page-specific book references for an even deeper learning experience!
DO YOU HAVE THE BOOK? ... NO???!!! ... STEP UP TO THE MAT! If you're interested in these upcoming DVDs, the book on which they are based is available in our online store! World-renowned teacher Jean Jacques Machado highlights the secrets behind gi and no-gi techniques for martial artists of all levels to successfully transition between styles.