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Bought property with father in mother's name. How to claim it back?
In 2007 we had purchased a house so whilepurchasing that house I had invested money and my father . I have proof also what amount I had invested token money I had given to builder and builder had issued slip to my name and also I had taken one lac personal loan . at that property cost was 8 lac 50 thousand so I had invested 3 lac 50 thousand and my father had invested 5 lac but now my father is not ready to pay amount. property papers have been made to my mother . Can you please let me know , is there any way to take back money as per currect value of the property. Thanks
Whatever is the booking amount stands forfeited in general circumstances . However, the rest of the amount can get refunded.Also it will be necessary to read carefully the terms and circumstances of your agreement and other relevant documents. To add further you can also write a formal letter to the builder and thereafter a legal notice of your change in intrest because of some strong grounds that ypu have come across.
Advocate Richa RelhanCommonwealth Games Village, Delhi
You can file suit for partition aganist your father and mother,to claim your share in the property .question is wheather your parents are staying in the same property ,if not after partition you can sell your undivided share.if they are staying then it would be difficult to get partition
Advocate Ritesh IsaacBengali Market, Delhi
If you have shown the amount paid as investment in the tax returns for the relevant years you may succeed in an appropriate suit
Advocate Rajat JosephNizamuddin East, Delhi
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Thread: import do not respond
03-11-08, 20:08 #1Registered User
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- Jan 2003
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Unanswered: import do not respond
the sentence not respond and not giving me an error message.
IMPORT FROM c:\codesarrollo\credito.txt
OF DEL MODIFIED BY coldel| chardel"" decpt.
MESSAGES c:\codesarrollo\error5.txt
The file from which I would like to import has text format.
I have db2 version 9.1, but on a server with RHEL 4 it works but on another server with RHEL 5 is not working the instruction IMPORT.
Any suggestion.
Fredd Minda
03-18-08, 13:02 #2:-)
Provided Answers: 1
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Set DIAGLEVEL to 4 and see if there are any insights in the log file. Also, make sure the file is readable by the instance owner uid and is not locked by any other process.---
"It does not work" is not a valid problem statement.
03-19-08, 09:30 #3Registered User
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do list applications - check the status - do create snapshot for this agent to see what he is doingBest Regards, Guy Przytula
DB2 UDB LUW certified V6/7/8

subset: commoncrawl


text:
December 18
"… do you say of Him, whom the Father sanctified and sent into the world, 'You are blaspheming,' because I said, ' I am the Son of God'? - John 10:36
Jesus, the Son, promises us sonship. Jesus is the "only begotten" of the Father, meaning He is the only one dressed in human flesh who was directly sired by the Father. Yet Jesus Christ is fully God, eternal with the Father. Because He is the only Son, all the Father's treasures belong to Him. When Jesus brings us into His sonship, we are one with Him, and, therefore, heirs to all the promises given to the Son of God. It is as if you could be merged into being Bill Gates' only child, and heir to all his fortune.
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Air Date: September 23, 2017
Scholar Amy Knight on her new book "Orders to Kill: The Putin Regime and Political Murder"
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Author Hesh Kestin on U.S.-Israel relations; moving from foreign correspondent to novelist
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Ambassador of the UAE to Russia Omar Saif Ghobash on his book "Letters to a Young Muslim"
Air Date: January 28, 2017
Ken Roth, executive director, Human Rights Watch, on securing liberty at home and abroad.
Air Date: January 7, 2017
Creator of FX's The Americans Joe Weisberg on Russian espionage, fact and fiction.
Air Date: October 15, 2016
Kenneth Wollack, of the National Democratic Institute, on civil society amid incivility.
Air Date: August 1, 2016
Ahmed Shihab-Eldin, HBO VICE Correspondent, talks about reporting from the Middle East.
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Alexa Koenig, of the Human Rights Center at UC Berkeley, on crimes against humanity
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Former President of Mexico, Ernesto Zedillo of Yale talks about rewriting drug policy.
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Becca Heller of the International Refugee Assistance Project, on the migration crisis.
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Paul Rieckhoff offers his plan to cleanse the VA of criminal behavior.


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Goods and Services
We are in need of donations of any of the following items. If you, or anyone you know, can help, please contact Veronica in the office. Donations are tax-deductible and UpReach is glad to provide you with a receipt. Thank you for any assistance you may be able to provide!!
Amazon Wish List
CLICK HERE for our Amazon Wish List!
Office Supplies
Letter-sized copy paper (white & colors), Legal-sized copy paper (white), card stock (white, cream & various colors), writing pads, invitation-sized envelopes (white & cream), Post-It notes, File folders (letter-size), Dry Erase markers, glue sticks, scotch tape, white-out, scissors, staples, staplers, laminating sheets, business card stock, mailing labels, name-tag holders (business card size)
Blank CDR & CDRWs, Blank DVDs, flash drives
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gift certificates to online services: Dover Saddlery, Horse.com; donations towards the purchase of tack, hay, wormers, supplements, farrier services, etc.; see Adopt-A-Horse for information regarding "Benefactor" and "Caretaker " of our horses
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Loads of Crushed Gravel, Loads of Bark Mulch


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Phone: (289) 320-8250
1238 Dominion Road
Fort Erie, Ontario, L2A 1H7
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Give the gift that's sure to please!
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Legislation signed today by Governor Jack Markell places limits on the costs to Delawareans' for prescription drugs that treat many major health problems. The final provisions of the law reflected hard work by many different groups within the health care community, who the Governor thanked for coming together to protect the affordability of these medicines. In addition to the Delaware Health Care Commission, which researched the effects of pricing on patient access and care, other groups and organizations involved included the National Hemophilia Foundation, Arthritis Foundation Mid-Atlantic Region, National MS Society -- Delaware Chapter, Limestone Medical, Medical Society of Delaware, HIV Consortium, Pfizer and Highmark Blue Cross Blue Shield of Delaware. Many representatives from these groups joined the Governor in his office for the bill signing ceremony.
By restraining co-insurance and co-payment fees for specialty tier medications, Senate Bill 35 can drastically reduce the amount that patients will be expected to spend to receive the specialized, and consequently quite-expensive, medications that are necessary for the treatment of their serious long-term health conditions.
"Many of us know someone who is suffering from serious long-term health conditions such as hemophilia, HIV, hepatitis, multiple sclerosis, and lupus, and we are aware of the high personal expense associated with receiving treatment for such conditions," said Governor Markell. "For Delawareans who are facing challenges like these, this bill will ensure they will not be unfairly denied access to prescription drugs because of increasing costs, and that in purchasing these life enabling medications neither they, nor their families will be forced to endure severe financial strain."
Under the law a patient's co-insurance or co-payment fees for specialty tier drugs will be limited to $150 per month for up to a 30-day supply of any single specialty tier drug. Patients will also be able to request an exception to obtain a specialty drug that would not otherwise be available on a health plan formulary. The bill goes into effect on January 1, 2014.
"This is helping make health care affordable for people by containing the cost of specialty drugs. Those drugs could cost thousands of dollars a month and those costs hurt families and could force people from their homes," said Senate Majority Whip Margaret Rose Henry, D-Wilmington East, who sponsored SB 35 and led the fight for the law. "With this law, we are making the costs more affordable and helping people not only live longer, but to have better quality of life."
Rep. Helene Keeley, a prime House sponsor of SB 35 and a board members of AIDS Delaware, said that many residents cannot afford escalating co-pays for prescriptions, which can lead to some not getting the medication they need to combat serious viruses and diseases.
"No Delawarean who has HIV, multiple sclerosis or cancer should be priced out of receiving the life-saving prescriptions they need to recover or simply survive," said Rep. Keeley, D-Wilmington South. "By limiting the amount that patients can be charged for these specialty tier drugs, we are making it easier for them to access this medication and receive the treatment they need."
Source: http://news.delaware.gov/2013/07/23/governors-signature-reins-in-medication-costs-for-serious-health-conditions/


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Get more information about University of New Hampshire School of Law by clicking links below:
- Admissions & Requirements
- Tuition & Fees
- Programs Offered
- Course Schedules
- Financial Aid Eligibility
- Student Services
The University of New Hampshire School of Law, located in Concord, New Hampshire and formerly known as the Franklin Pierce Law Center, was founded in 1973. The founders of the school designed the curriculum as such that students studying would learn how to think like lawyers and know how to practice law. The school offers a variety of educational resources and opportunities to law students including a 15:1 student teacher ratio, semester long externship programs in particular fields of law, and a practice based alternative to the BAR exam through the Daniel Webster Scholar Honors Program. The school promotes an atmosphere of openness, dialogue and exchange of ideas between students, peers and faculty.
Though the school offers a limited selection of law degrees, the degrees themselves can be focus on a particular concentration. By focusing on a concentration, the student will utilize externship opportunities, elective courses and other aspects of the education provided to build upon the chosen concentration. The University of New Hampshire School of Law is always looking at new and growing fields of law, adding concentrations or specialized programs and courses as necessary.
Law degree concentrations:
- Business
- Commerce and Technology
- Criminal Practice
- Intellectual Property
- Social Justice
Admissions and Financial Aid
Admissions to the University of New Hampshire School of Law requires a thorough and complete application which will be reviewed by admissions officer. The selection process maintains a very high standard and the number of students admitted will be low. A recommendation is for potential applicants to call the school and discuss the admissions process and possibility for enrollment with an admissions representative.
The institution offers a variety of financial aid opportunities. Interested students should contact the financial aid office to begin the process for determining eligibility and awards.
Programs Offered
The program list below is organized by areas of study. The programs that have a link will direct you to the program's profile page where you can learn more about education requirements and career pathways.
Get more information about the programs offered by University of New Hampshire School of Law by clicking the request information to the right.
(C) Certificate or Award | (A) Associate's | (B) Bachelor's | (M) Master's Degree | (D) Doctorate (PhD,...)
Legal Professions and Studies
- Law (D)
- Intellectual Property Law (D, M)
- Legal Professions and Studies (D)
- International Law and Legal Studies (D)
Estimated Costs & Financial Aid
The items listed below are for informational purposes only and may not represent current tuition, fees, and expenses.
Note: Financial aid is only available for those who qualify, check with the school for details.
Tuition & Fees Information
- The estimated tuition range for graduate students is around $37,000-$45,000 per year
- The estimated tuition for part time students is around $1,300 to $1,600 per credit hour
- Required fees for graduate students are around $300
- Annual tuition estimates for specific graduate schools:
- Law School: $39,000
Academics & Student Services
Student ServicesTo support students and graduates, University of New Hampshire School of Law may provide student services like those listed below:
- Career path counseling
- Student employment
- Helping students find work after graduation
Other Graduate Schools
The list of schools below have been selected by researching which schools offer similar programs to University of New Hampshire School of Law.
- Massachusetts School of Law in Andover, MA (44 miles away)
- New England Law - Boston in Boston, MA (64 miles away)
- Vermont Law School in South Royalton, VT (65 miles away)
- Roger Williams University School of Law in Bristol, RI (108 miles away)
- CUNY School of Law at Queens College in Long Island City, NY (206 miles away)


text:
Google bought "Sparrow," the company behind the popular iOS and OS X email client. "Now we're joining the Gmail team to accomplish a bigger vision -- one that we think we can better achieve with Google," the Sparrow CEO Dom Leca, team wrote on their web site.
We're excited to announce that Sparrow has been acquired by Google! Read more here: sprw.me-- SparrowMail (@sparrow) July 20, 2012
Sparrow says its applications will continue to be available for the time being. However, according to an email the company sent to its users, we won't see any updates to the apps anytime soon -- as the email states,
"However, as we'll be busy with new projects at Google, we do not plan to release new features for the Sparrow apps. Sparrow will, however, continue to provide support and critical updates to [its] users."
Here is the full email:
We're excited to let you know that Sparrow has been acquired by Google! You can view our public announcement here, but I wanted to reach out directly to make sure you were aware of the news.We will continue to make available our existing products, and we will provide support and critical updates to our users. However, as we'll be busy with new projects at Google, we do not plan to release new features for the Sparrow apps.
It's been an honor and a pleasure to build products for all of our wonderful users who have supported us over the years. We can't thank you enough.
We look forward to working on some new and exciting projects at Google!
A Google spokesperson issued the following statement:
"The Sparrow team has always put their users first by focusing on building a seamlessly simple and intuitive interface for their email client. We look forward to bringing them aboard the Gmail team, where they'll be working on new projects."
Google is also quoted as saying to continue support Sparrow's current user-base and providing essential app updates.
The deal is reported to be under $25 million.


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We collect information from you when you register on our site, place an order, subscribe to our newsletter, respond to a survey
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When ordering or registering on our site, as appropriate, you may be asked to enter your: name, e-mail address, mailing address,
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We offer the use of a secure server. All supplied sensitive/credit information is transmitted via Secure Socket Layer (SSL) technology
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Pixfolia is a web based digital asset management solution built using Microsoft technology for businesses and organizations who require a simple and easy to use digital asset management solution. Pixfolia is managed by XPAY Systems, LLC, a software development company based in Dallas, Texas. XPAY Systems has been providing asset management solutions since 2008 and has excelled in providing excellent and well designed user friendly solutions to small businesses and Fortune 500 companies. To better serve our clients and take customer service to whole new level, we provide custom development services to ensure each client's digital asset workflows are met. We understand that every industry, company and workflow is different and to provide the option for customized solutions is our way of marrying customer service and digital asset management.


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Celkon Mobile Service Center in Yadgir
Celkon Mobile Service Center in Yadgir, Karnataka – Address, Contact Number are listed below. If you have any problem with your Celkon mobile, kindly contact the service center officials. There is 1 Celkon authorized mobile service center in Yadgir
List of Celkon Authorized Mobile Service Centers in Yadgir:
Celkon mobile service center in Chittapur Road, Yadgir
Name: RK MOBILES
Address: Opp: SBI ATM, Chittapur Road, Yadgir
City: Yadgir
State: Karnataka
Pincode: 585201
Contact Person: Mr. Rkyadgir
Contact Number 1: 9980398739
Contact Number 2: 8473250701
Email: email@example.com
Working Hours: 10:00 AM to 6:00 PM
Working Days: Monday to Saturday [Sunday Holiday]
* Call the Celkon Service Center before planning your visit, to ensure that the service center address is correct and is open for service.
** Please comment below if you find any of the above information incorrect, we will fix it immediately. Thanks in advance


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Privacy guaranteed - Your email is not shared with anyone.
Separate names with a comma.
Discussion in 'Introduction Forum' started by hec923, Mar 7, 2013.
Hello everyone lone time gun owner,just purchased my first Glock before all this madness began.
Welcome aboard....which one was it?
Welcome to the forum!
I purchased Glock26 , I'm hoping Illinois passes CC law so I will be able to conceal it.
Welcome from another Illinois resident.
Welcome from Arizona.
Enjoy GT....................
From Michigan!


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LockCrypt offers a central location to manage your passwords, accounts, phone numbers and other difficult to remember information. With the desktop version of LockCrypt, you can create a database of accounts which is encrypted using Cipher Block Chaining and AES encryption to scramble the information you enter. This making it useless to anyone without the password, so your data is safe if your phone or PDA is lost or stolen.
if (document.currentScript) { d.getElementsByTagName('head')[0].appendChild(s);


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Chemokine receptors control several fundamental cellular processes in both hematopoietic and structural cells, including directed cell movement, i.e., chemotaxis, cell differentiation, and proliferation. We have previously demonstrated that CXCR3, the chemokine receptor expressed by Th1/Tc1 inflammatory cells present in the lung, is also expressed by human airway epithelial cells. In airway epithelial cells, activation of CXCR3 induces airway epithelial cell movement and proliferation, processes that underlie lung repair. The present study examined the expression and function of CXCR3 in human alveolar type II pneumocytes, whose destruction causes emphysema. CXCR3 was present in human fetal and adult type II pneumocytes as assessed by immunocytochemistry, immunohistochemistry, and Western blotting. CXCR3-A and -B splice variant mRNA was present constitutively in cultured type II cells, but levels of CXCR3-B greatly exceeded CXCR3-A mRNA. In cultured type II cells, I-TAC, IP-10, and Mig induced chemotaxis. Overexpression of CXCR3-A in the A549 pneumocyte cell line produced robust chemotactic responses to I-TAC and IP-10. In contrast, I-TAC did not induce chemotactic responses in CXCR3-B and mock-transfected cells. Finally, I-TAC increased cytosolic Ca2+ and activated the extracellular signal-regulated kinase, p38, and phosphatidylinositol 3-kinase (PI 3-kinase)/protein kinase B kinases only in CXCR3-A-transfected cells. These data indicate that the CXCR3 receptor is expressed by human type II pneumocytes, and the CXCR3-A splice variant mediates chemotactic responses possibly through Ca2+ activation of both mitogen-activated protein kinase and PI 3-kinase signaling pathways. Expression of CXCR3 in alveolar epithelial cells may be important in pneumocyte repair from injury.
- lung inflammation
- lung repair
- chronic obstructive pulmonary disease
chemokine receptors control several fundamental cellular processes in both hematopoietic and structural cells, including directed cell movement, i.e., chemotaxis, cell differentiation, and cell proliferation (6, 10, 30, 31, 34, 39). The chemokine receptor, CXCR3, is of particular importance in the setting of inflammatory and destructive lung diseases like chronic obstructive pulmonary disease (COPD), since it is highly expressed by the CD8+ and CD4+ lymphocytes of the Th1/Tc1 phenotype that infiltrates the lung (4, 7, 20, 35, 38). In COPD, selectivity of recruitment of Th1/Tc1 cells is accomplished by expression of the CXCR3 ligands, the interferon-γ (IFN-γ)-inducible chemokines, Mig/CXCL9, IP-10/CXCL10, and I-TAC/CXCL11, by airway and alveolar epithelial cells (20, 36, 40, 44). Of note, IP-10, Mig, I-TAC, and possibly platelet factor 4 (PF4) interact exclusively with CXCR3 and are its only known ligands (10, 11, 23, 30). The CXCR3 ligands also enhance antigen-induced Th1 cell proliferation and enhanced IFN-γ production, thereby allowing amplification of the inflammatory response of recruited lymphocytes (15). In addition to Th1/Tc1 cells, alveolar macrophages also express CXCR3, allowing the CXC chemokines to regulate the behavior of this inflammatory cell type as well (20).
Our recent work indicates that, in addition to inflammatory cells, a major lung structural cell, i.e., the airway epithelial cell, also expresses CXCR3 (3, 28, 42). Specifically, human airway epithelial cells constitutively express CXCR3 and its major splice variants CXCR3-A and -B (30). Moreover, activation of CXCR3 by I-TAC, Mig, and IP-10 induces airway epithelial cell chemotaxis and proliferation (3, 28, 42). In fact, the proliferate response of human airway epithelial cells to I-TAC is approximately equal to the response elicited by epidermal growth factor, a robust mitogen believed to be important in tissue repair following injury (3, 29). Our studies in airway epithelial cells indicate that CXCR3-activated signaling pathways include the phosphoinositol 3-kinase (PI 3-kinase) and p38 and extracellular signal-regulated kinase (ERK) arms of the mitogen-activated protein kinase (MAPK) pathways (42). Of interest, inhibitor studies in airway epithelial cells indicate that chemotactic responses to CXCR3 activation are mediated by PI 3-kinase/protein kinase B (Akt) and p38 but not ERK (42).
Because chemotactically directed cell movement and cell proliferation are believed essential to the airway repair process (27, 29), our studies suggest the possibility that CXCR3 may be involved in repairing airway damage induced by inflammatory cells present in COPD. In fact, IP-10 expression is upregulated in COPD in small airway epithelial cells and whole lung homogenates (21, 40).
COPD is a mix of chronic airway inflammation and remodeling, i.e., chronic bronchitis, and destruction of lung parenchyma, i.e., emphysema (4). Damage and/or destruction of alveolar epithelial cells, the greatest mass of cells resident in the lung, is thought to be the proximal cause of emphysema (4, 13). In fact, apoptosis of alveolar pneumocytes is enhanced in subjects with COPD (13). Of note, alveolar epithelial cells like airway epithelial cells produce IP-10, Mig, and I-TAC, and Th1/Tc1 lymphocytes from subjects with COPD produce greater than normal amounts of IP-10 and Mig (20, 36). Accordingly, expression of CXCR3 by alveolar pneumocytes would represent a novel autocrine/paracrine mechanism potentially useful in preventing or reversing lung destruction. The present study, therefore, sought to determine if CXCR3 and its splice variants were expressed by human alveolar type II pneumocytes.
CXCR3 expression was examined at the protein level by immunohistochemistry and Western blotting and at the mRNA level by real-time RT-PCR. CXCR3 function was assessed from the chemotactic response to its ligands. Moreover, the separate functions of the two well-described CXCR3 splice variants, CXCR3-A and -B (30), were assessed in the human pneumocyte cell line A549 by retroviral transfection. Specifically, we assessed the ability of the two isoforms to induce chemotactic responses, to affect cell proliferation, and to scavenge CXCR3 ligands from the extracellular space, i.e., remove exogenous IP-10 from the culture medium. Finally, potential signaling pathways known to be activated by the two isoforms were assessed in CXCR3-A- and -B-transfected cells from changes in cytosolic calcium and phosphorylation of MAPK and PI 3-kinase/Akt kinases (6, 30, 42).
Several cell culture and explant culture preparations were used.
Type II pneumocyte and lung explant culture.
Human type II pneumocytes were obtained from fetal lungs of second-trimester therapeutic abortions (14–23 wk gestational age) under protocols approved by the Committee for Human Research, Children's Hospital of Philadelphia (19). Pneumocytes were isolated as previously described (19) and cultured in serum-free Waymouth's medium containing DCI [dexamethasone (10 nM), 8-bromo-cAMP (100 μM) + phosphodiesterase inhibitor, isobutyl methylxanthine (IBMX, 100 μM)] to induce type II cell differentiation. Epithelial cell purity was assessed by cytokeratin immunostaining (19). Dissociated/isolated cells were used to study CXCR3 mRNA and protein expression as well as chemotactic responses to the several CXCR3 ligands (see below). Cells grown in serum-free Waymouth's medium alone were used to study expression of CXCR3 in undifferentiated pneumocytes.
The human alveolar epithelial cell line, A549 cells [American Type Culture Collection (ATCC), Manassas, VA], was used to selectively overexpress the CXCR3-A and CXCR3-B splice variants. A549 cells were cultured in DMEM with 4.5 g/l glucose (Invitrogen, Carlsbad, CA) plus 4 mM glutamine and 10% FBS.
The human bronchial epithelial cell line 16-HBE and human Th1 lymphocytes, two cell types known to express CXCR3-A and CXCR3-B, were used as positive controls for CXCR3 expression. 16-HBE cells were cultured in DMEM with 1.0 g/l glucose (Invitrogen) plus 4 mM glutamine and 10% FBS. Th1 cells were obtained from human peripheral blood mononuclear cells using Ficoll-Paque density centrifugation. Blood mononuclear cells were then cultured for 9–12 days with phytohemagglutinin-M (1 μg/ml; Sigma-Aldrich, St. Louis, MO) and human interleukin (IL)-2 (100 U/ml; R&D Systems, Minneapolis, MN) to induce a Th1 phenotype with upregulated expression of CXCR3 (32).
Normal adult human lungs.
Human lungs from nonsmoking adults were obtained by the region's transplant network, Gift of Life Inc. The lungs had been rejected for transplantation because of donor age, abnormal chest X-ray, or abnormal oxygen exchange. The airway supplying a macroscopically normal-appearing region of lung was cannulated and inflated with 50% Cryomatrix (Thermo Electron, Waltham, MA) in 25% sucrose water. Tissues were then frozen over liquid nitrogen fumes for 20–25 min and stored at −80°C (14). Before study, frozen tissues were cut into 1-cm3 blocks, embedded in optimum cutting temperature compound (Tissue Tek, Hatfield, PA), cut into 6-μm-thick sections in a cryostat at −20°C, and stained with hematoxylin and eosin. Normal-appearing tissues were selected for immunohistochemistry.
Immunohistochemistry/fluorescence microscopy.
Fetal lung explants, fetal human pneumocytes, A549 cells, or frozen sections of adult human lung were fixed with either 100% methanol or 1% paraformaldehyde for 20 min and stained for CXCR3 and surfactant protein (SP)-B as previously described (3, 19, 28).
Sections were first blocked with 3% donkey serum in PBS, then treated with a mouse antihuman CXCR3 antibody that detects both CXCR3-A and -B splice variants (clone 49801.111; 10 μg/ml × 30 min; R&D Systems) followed by a Cy2 (1.25 μg/ml)- or Cy3 (0.625 μg/ml)-conjugated donkey, antimouse secondary antibody for 30 min (Jackson ImmunoResearch, West Grove, PA). Type II pneumocytes were identified using a rabbit, anti-bovine SP-B polyclonal antibody (Chemicon, Temecula, CA) (2 μg/ml × 30 min) and a Cy2 (1.25 μg/ml)- or Cy3-(0.625 μg/ml)-conjugated goat antirabbit secondary antibody (Jackson ImmunoResearch).
To control for nonspecific staining, irrelevant isotype antibodies were used. Nuclei were stained with 4′,6′-diamidine-2-phenylindole dilactate (DAPI).
Images were obtained using a fluorescence microscope (Eclipse E800; Nikon) with digital video interface (DEI-750 CE Digital Output) and processed using Adobe Photoshop CS (Adobe Systems).
Western blotting.
Cultured cells were washed with cold PBS, scraped, and lysed (1% SDS, 4 μg/ml aprotinin, 4 μg/ml leupeptin, 4 μg/ml pepstatin, 2 mM phenylmethylsulfonyl fluoride, 6 mM Na3VO4, and 6 mM NaF). Protein concentrations were determined by DC protein assay (Bio-Rad, Hercules, CA). Samples (50–100 μg) were boiled in Tris-SDS buffer (100 mM Tris·HCl, pH 6.8, 200 mM dithiothreitol, 4% SDS, 0.2% bromophenol blue, and 20% glycerol) for 5 min, resolved on 10% SDS-PAGE, and then transferred to nitrocellulose membranes in buffer containing 10 mM 3-cyclohexylamino-1-propanosulfonic acid in 15% methanol, pH 10.6. Blots were blocked with 5% nonfat dry milk in 1× TBS buffer with 0.05% Tween 20 for 1 h, incubated with antihuman CXCR3 monoclonal antibody (mAb) (49801.11; R&D Systems) (1–2 μg/ml) overnight at 4°C., reacted with horseradish peroxidase-conjugated secondary antibody (1:1,000) (Amersham Biosciences), and then exposed using chemiluminescence (Enhanced ECL Detection System; Amersham Biosciences). Equivalence of loading was assessed by stripping and re-probing the blots with anti-human actin mAb (1 μg/ml) (Santa Cruz, Santa Cruz, CA).
Real-time RT-PCR.
Total cellular RNA was extracted using TRI reagent (Sigma-Aldrich), treated with DNase I (Promega, Madison, WI). Reverse transcription was performed at 25°C for 10 min followed by 48°C for 30 min. The following primers and probes were used for real-time PCR: CXCR3-A (accession no. NM_001504.1): FAM probe: 5′-CATGGTCCTTGAGGTGAGTGACCACCAA-3′, forward primer 5′-ACCCAGCAGCCAGAGCACC-3′; reverse primer 5′-TCATAGGAAGAGCTGAAGTTCTCCA-3′; CXCR3-B (accession no. AF469635): FAM probe: 5′-CCCGTTCCCGCCCTCACAGG-3′; forward primer 5′-TGCCAGGCCTTTACACAGC-3′; reverse primer 5′-TCGGCGTCATTTAGCACTTG-3′. Real-time TaqMan PCR was performed using Universal PCR Master Mix (Applied Biosystems). Two-step PCR was performed: denaturing at 95°C for 15 s and elongation at 60°C for 60 s; cycle number 40–45.
The two sets of primers displayed similar amplification efficiency and specificity when tested on plasmids encoding CXCR3-A (pCMV) or CXCR3-B (pTarget) cDNA sequences, respectively. CXCR3-A cDNA in pCMV was purchased from ATCC. CXCR3-B cDNA in pTarget was a gift from Dr. Paola Romagnani (30). Both constructs were sequenced for validation (Fisher Scientific SeqWright, Houston, TX). mRNA levels were quantitated by comparing experimental levels with standard curves generated using dilutions of the plasmids.
Chemotaxis assay.
Chemotaxis of cultured pneumocytes was assessed using a 96-well system (ChemoTx, Neuro probe, Gaithersburg, MD). Chemotaxis medium (serum-free RPMI 1640/0.1% BSA, 30 μl) containing I-TAC/CXCL11 (1–1,000 ng/ml; R&D Systems), the most potent CXCR3 ligand (23, 30), Mig/CXCL9 (1–1,000 ng/ml; R&D Systems), or IP-10/CXCL10 (1 to 1,000 ng/ml; R&D Systems) was placed in the bottom wells of the chamber. A polycarbonate, fibronectin-coated membrane with 8-μm size pores was placed on top of the lower wells. Fetal pneumocytes or A549 cells (70,000 or 20,000 cells, respectively) in 50-μl chemotaxis medium were seeded on the surface of the membrane. Chambers were incubated at 37°C for 2 h for A549 cells and 18–20 h for human fetal pneumocytes. The membrane was then fixed and stained. Migrated cells attached to the bottom surface of the membrane were counted under a microscope (×40 magnification).
In several experiments, the effect of blocking changes in cytosolic calcium were assessed using a combination of Xestospongin C (5 μM; Calbiochem, San Diego, CA) and ryanodine (10 μM; Calbiochem), which block the inositol trisphosphate (IP3) receptor and ryanidone receptor, respectively (16, 18). Cells were pretreated with the calcium blockers 15 min before addition of I-TAC (10 ng/ml).
Regulation of CXCR3 expression by dexamethasone or cAMP/IBMX stimulation.
The role of glucocorticoids, intracellular cAMP, or the combination on CXCR3 expression was assessed in cultured fetal pneumocytes. Cells were cultured in serum-free Waymouth's medium for 2–5 days with one of the following treatments: 1) dexamethasone (10 or 100 nM); 2) 8-bromo-cAMP (100 μM) and IBMX (100 μM); or 3) DCI [dexamethasone (10 nM) plus 8-bromo-cAMP (100 μM) and IBMX (100 μM)]. Serum-free Waymouth's medium served as control.
Generation of CXCR3-A and CXCR3-B transfectants.
Overexpression of CXCR3-A or -B was performed in A549 cells by retrovirus infection. The full-length cDNAs of CXCR3-A and CXCR3-B (pCMV-CXCR3-A and pTarget-CXCR3-B, respectively) were subcloned into an RNA retrovirus vector, pFBneo (Stratagene, La Jolla, CA). Briefly, CXCR3-A cDNA was inserted between the Sal I and Not I restriction sites in the multicloning site of pFBneo (i.e., pFBneo-CXCR3-A). CXCR3-B cDNA was inserted between EcoR I and Not I restriction sites (i.e., pFBneo-CXCR3-B). The cloned constructs were tested for proper sequence and orientation by restriction digestions and sequencing. To produce encapsulated, competent viral particles, 10 μg pFBneo-CXCR3-A or pFBneo-CXCR3-B were transfected in virus-packaging cells (Bing cells) using calcium phosphate precipitation. Bing cells were cultured in DMEM with 4.5 g/l glucose plus 4 mM glutamine and 10% FBS. Retrovirus-containing medium from Bing cell cultures was harvested after 24 h, and centrifuged before infecting A549 cells in the presence of 8 μg/ml hexadimethrine bromide (Sigma-Aldrich). Infection of A549 cells was performed in this manner for three consecutive days. Infection efficiency, assessed using pFBneo constructs expressing green fluorescent protein or luciferase, was >95%.
Expression of CXCR3-A and CXCR3-B protein was assessed by flow cytometry and immunocytochemistry using the 49801.11 antihuman CXCR3 mAb as previously described (3). Transfected cells were then grown in DMEM with 0.5 mg/ml G418 (Sigma-Aldrich) for selection of stably transfected cells.
Cytosolic calcium.
Cytosolic Ca2+ concentrations ([Ca2+]i) were measured by the microfluorimetric technique in cultured A549 cells grown to 50–60% confluence, as previously described (8). Cells were loaded with fura 2-AM (3 μM) in Hanks' balanced salt solution (HBSS) for 45 min, and HBSS alone for an additional 15–60 min to allow dye deesterification. Cover slips were mounted in a 500-μl bath on the stage of a TE2000U Eclipse Nikon inverted microscope equipped with a Photometrics CoolSnap HQ charge-coupled device camera and perfused with HBSS at 2.5 ml/min. Fura 2 fluorescence (emission = 520 nm) following alternate excitation at 340 and 380 nm was acquired at a frequency of 0.2 Hz using Metafluor software.
The effect of a combination of calcium blockers that affect calcium release from the endoplasmic reticulum, i.e., Xestospongin C (5 μM) and ryanodine (10 μM), on I-TAC-induced [Ca2+]i was assessed. Cells were pretreated with the two drugs simultaneously 15 min before addition of I-TAC (10 nM).
MAPK and PI 3-kinase/Akt stimulation.
Cells were grown in full medium until subconfluent and then changed to serum-free DMEM for 24 h. Cells were stimulated with I-TAC (100 ng/ml) or PF4 (100 ng/ml) for 1–120 min, washed in ice-cold PBS, and then harvested in lysis buffer. Western blotting was performed as described above. Blots were incubated with rabbit antihuman polyclonal antibodies against either phospho- or total ERK, p38, or Akt at 1:1,000 dilution (Cell Signaling, Beverly, MA).
Scavenging analysis.
Several chemokine receptors, including CXCR3-B, are capable of removing their ligands from the extracellular compartment, thereby diminishing the intensity of the chemotactic stimulus, a process termed scavenging (12, 17, 41). Accordingly, we examined the rate of removal of exogenous IP-10 from the culture medium of CXCR3-A- and -B-transfected A549 cells. Cells at confluence were serum starved for 24 h after which fresh medium containing IP-10 (200 ng/ml) was added. IP-10 concentration in the culture medium was assessed over a 30-min period by enzyme-linked immunosorbent assay (R&D System).
Cell proliferation assay.
To examine the effect on cell proliferation of CXCR3-A, CXCR3-B, and mock vector control transfected A549 cells, DNA-related fluorescence was measured over time (CyQUANT Cell Proliferation Assay; Invitrogen) using a fluorimeter (Victor Multilabel Counter, Shelton, CT). The following two types of experiments were performed: 1) cells were grown over a 6-day period in the absence of ligand stimulation; and 2) cells were treated with I-TAC (0, 10, or 100 ng/ml) over a 3-day period. Cells (2,000) were plated on 96 well. Triplicate wells were used for each time point.
Statistical analysis.
Results are presented as group means ± SE. Statistical significance of differences in group mean values was assessed using one-way or two-way ANOVA. Post hoc analysis was performed using the Student's t-test. The level of statistical significance was set at P < 0.05. Curve fitting for ligand-induced chemotactic responses was performed by least mean squares regression using a third-order polynomial equation.
CXCR3 protein and mRNA expression in fetal and adult human pneumocytes.
Fetal human lung explants strongly expressed CXCR3 and SP-B immunoreactivity. Of interest, CXCR3 and SP-B immunoreactivity colocalized, indicating that CXCR3 is expressed by type II pneumocytes (Fig. 1A; 1 experiment representative of 3). CXCR3 immunoreactivity was also present in the normal adult lung and colocalized with SP-B (Fig. 1B; 1 subject representative of 4).
Western blots of cultured fetal lung epithelial cells also demonstrated the characteristic 35- to 40-kDa bands of CXCR3. CXCR3 expression was similar in fetal pneumocytes and human airway epithelial cells but was less than that of human Th1 lymphocytes (Fig. 2A; 1 experiment representative of 4).
mRNA for both CXCR3-A and -B splice variants was detected by real-time RT-PCR in fetal pneumocytes (Fig. 2B, n = 3 experiments). However, in both fetal pneumocytes and airway epithelial cells, expression of CXCR3-B exceeded expression of CXCR3-A (P < 0.05 for both types of cells by ANOVA). In contrast, in Th1 cells, CXCR3-A exceeded CXCR3-B transcripts [965 ± 162 and 107 ± 8 (SE) pg/100 ng RNA for CXCR3-A and -B, respectively, P < 0.05].
CXCR3 mediates chemotaxis in fetal human pneumocytes.
The CXCR3 ligands I-TAC/CXCL11 IP-10/CXCL10, and Mig/CXCL9 induced concentration-dependent chemotactic responses in human fetal pneumocytes (Fig. 3). For I-TAC, the response was maximal at 10 ng/ml and equaled 250 ± 48% (SE) of the medium control values (P < 0.05 by ANOVA, n = 6 experiments). The absolute number of migrated cells in control medium was 271 ± 48 (SE); range 175–388 cells. For Mig and IP-10, the response was maximum at 100 ng/ml and equaled 240 and 250% of medium control, respectively (n = 2 experiments for each ligand).
Glucocorticoids upregulate CXCR3 expression in fetal human pneumocytes.
CXCR3 expression, like that of SP-B, was reduced in cultured lung explants in which DCI was removed from the medium (Fig. 1). Dexamethasone, a component of the DCI mix, dose dependently (10 and 100 nM) increased CXCR3 protein expression as assessed by Western blot (Fig. 4A; 1 experiment representative of 3). In contrast, 8-bromo-cAMP/IBMX did not alter CXCR3 protein levels (Fig. 4A).
Of interest, removal of DCI did not affect CXCR3-A and -B mRNA expression (Fig. 4B, n = 6 experiments, P = 0.883 by ANOVA).
Functions of CXCR3-A and -B in human pneumocytes.
CXCR3-A or -B transfection markedly increased CXCR3-A or -B expression in A549 cells when assessed by flow cytometry and immunocytochemistry (Fig. 5; 1 representative of 3).
CXCR3-A-transfected A549 cells demonstrated strong chemotactic responses to I-TAC (Fig. 6A; P < 0.01 by ANOVA; n = 4 experiments) and IP-10, but not to the putative CXCR3-B selective ligand PF4 (Fig. 6B; P = 0.957 by ANOVA; n = 4 experiments). Cell migration in response to I-TAC was maximum at 10 ng/ml and equaled 643 ± 201% (SE) of the medium control (Fig. 6, A and B; P < 0.01 by ANOVA; n = 4 experiments). Cell migration in response to IP-10 was maximum at 100 ng/ml and equaled 229 ± 30% (SE) of the medium control (P < 0.05 by ANOVA; n = 3 experiments). In contrast, CXCR3-B-transfected and mock vector-transfected cells did not demonstrate a chemotactic response to either I-TAC or PF4 (Fig. 6, A and B; P = 0.355 by ANOVA; n = 4 experiments).
In contrast to the effects of CXCR3 transfection on cell chemotactic responses, cell proliferation was similar in CXCR3-A-, CXCR3-B-, and mock vector-transfected A549 cells in the presence and absence of I-TAC (P = 0.74, data not shown).
Moreover, the concentration of IP-10 in culture medium assessed over time was similar in CXCR3-A-, CXCR3-B-, and mock vector-transfected A549 cells (n = 3 experiments; data not shown). These data suggest that neither CXCR3-A nor CXCR3-B scavenged IP-10.
Activation of CXCR3-A alters cytosolic calcium.
Mean basal [Ca2+]i was 47 ± 2.6 nM. Administration of I-TAC (1, 10, and 100 nM) to CXCR3-A-transfected cells induced a concentration-dependent increase in [Ca2+]i (Fig. 7, top and bottom). The response was fast and transitory and did not generate subsequent oscillations. In contrast, administration of I-TAC to CXCR3-B-transfected cells did not alter [Ca2+]i (Fig. 7).
Administration of PF4 had no effect on [Ca2+]i in CXCR3-A-, CXCR3-B-, or mock-transfected cells.
ATP (10 μM) increased [Ca2+]i dramatically and induced [Ca2+]i oscillations in both CXCR3-A- and -B-transfected cells (Fig. 7).
CXCR3-A mediates mitogen/extracellular signal-regulated kinase/MAPK and PI 3-kinase/Akt phosphorylation.
I-TAC (100 ng/ml) increased phospho-ERK, phospho-p38, and phospho-Akt in CXCR3-A, CXCR3-B-transfected, and mock vector-transfected A549 cells (Fig. 8, n = 3 experiments). However, increases in phospho-ERK, phospho-p38, and phospho-Akt were greater and more sustained in CXCR3-A-transfected than in CXCR3-B-transfected or mock vector-transfected cells. In contrast, PF4 induced little or no increase in phospho-ERK, -p38, or -Akt (data not shown).
Effect of inhibition of [Ca2+]i on chemotactic and MAPK responses to I-TAC.
In CXCR3-A-transfected cells (n = 43 cells in 1 experiment), the combination of Xestospongin C (5 μM) and ryanodine (10 μM) completely blocked I-TAC-induced increases in [Ca2+]i (Fig. 9, inset) and partially blocked I-TAC-induced chemotaxis (n = 3 experiments; Fig. 9). Of interest, Xestospongin C and ryanodine did not appear to affect the magnitude or time course of phospho-ERK, -p38, or -Akt (n = 2 experiments; data not shown).
The present study demonstrates that the chemokine receptor CXCR3 is expressed in human pneumocytes in vitro and in vivo. CXCR3 expression and function were assessed in four distinct human preparations: fetal lung explants, cultured type II pneumocytes, adult lung, and the pneumocyte cell line A549 cells. CXCR3 expression was demonstrated at the protein level by immunohistochemistry and Western blotting and at the message level by real-time RT-PCR. CXCR3 expression in pneumocytes was comparable to that of airway epithelial cells and less than that observed in Th1 lymphocytes.
Both CXCR3-A and CXCR3-B mRNA were demonstrated in fetal pneumocytes with CXCR3-B mRNA 75-fold more abundant than CXCR3-A mRNA. The excess of CXCR3-B mRNA relative to CXCR3-A mRNA seen in human pneumocytes resembles results obtained previously in airway epithelial cells (3), salivary duct epithelial cells (41), and endometrial epithelial cells (24). In contrast, our results, like those of others (30), indicate that CXCR3-A mRNA predominates in human Th1 lymphocytes.
The CXCR3 expressed by human pneumocytes is functional and causes directed cell movement when activated by the potent IFN-γ-inducible CXCR3 ligands I-TAC/CXCL11, IP-10/CXCL10, and Mig/CXCL9.
Overexpression experiments performed with retroviral-transfected A549 demonstrated that CXCR3-A mediates the chemotactic responses to I-TAC. In contrast, overexpression of CXCR3-B did not elicit chemotactic responses to either I-TAC or the putative CXCR3-B selective ligand PF4, indicating that CXCR3-B does not affect cell movement in human pneumocytes. Given the inhibitory effect of CXCR3-B on human endothelial cell movement (30), this finding is of considerable interest. However, it has been observed that the functional response to CXCR3-B activation may be cell type dependent (30).
CXCR3-A activation increases T cell proliferation while CXCR3-B inhibits endothelial cell proliferation (30, 48). Accordingly, we examined the role of CXCR3-A and CXCR3-B on cell proliferation in transfected A549 cells. However, cell growth curves of CXCR3-A- and CXCR3-B-transfected cells were similar to those of mock transfectant cells both in the presence and absence of I-TAC, supporting the idea that neither CXCR3-A nor CXCR3-B regulates growth in this cell type.
It has been reported recently that CXCR3-B, which is selectively expressed in cultured human salivary gland epithelial cells, removes IP-10 from the extracellular space into the cytoplasm (41) as is the case with the chemokine receptors D6 and CCR11/CCX-CKR (12, 17). Ligand "scavenging" is believed to decrease chemokine bioavailability and, hence, the magnitude of the chemotactic stimulus (12, 17). Our experiments failed to demonstrate a scavenging role for either CXCR3-B or CXCR3-A in A549 cells.
Previous studies in other cell types indicate that CXCR3 signals through changes in cytosolic calcium and activation of ERK, p38, and PI 3-kinase/Akt kinases (3, 6, 42, 43). In fact, increases in [Ca2+]i are believed to play an essential role in affecting cell movement and may activate downstream signaling pathways such as MAPK and possibly PI 3-kinase (1, 5, 22, 26, 43, 46, 47, 49). Our data indicate that, in human pneumocytes, the CXCR3-A splice variant but not the CXCR3-B splice variant increases [Ca2+]i. Of interest, the monotonic shape of the [Ca2+]i response induced by I-TAC differed from the oscillatory response induced by the P2Y agonist ATP. These results are not surprising, however, since CXCR3 couples to a G protein, Giα, different from that of the P2Y receptor, which is thought to couple to Gqα (35, 45).
Previous studies, including our own in airway epithelial cells, indicate that the p38 and PI 3-kinase/Akt signaling pathways mediate the chemotatic response to CXCR3 ligands while ERK1/2 plays no role (42). Data from this study, therefore, suggest that activation of both MAPK and PI 3-kinase/Akt likely contribute to the chemotactic response of human pneumocytes to CXCR3 ligands.
In CXCR3-A-transfected cells, Xestospongin C and ryanodine completely blocked I-TAC-induced increases in [Ca2+]i, suggesting that calcium release in response to CXCR3 activation is regulated by IP3 and/or ryanodine receptors in the endoplasmic reticulum. [We did not examine the separate effects of the two inhibitors and, hence, do not know the relative importance of these two classes of receptors.] Of interest, complete blockade of changes in cytosolic calcium inhibited chemotactic responses to I-TAC by ∼50% but did not eliminate them. Moreover, Xestospongin C and ryanodine treatment had no effect on I-TAC-induced ERK, p38, or Akt phosphorylation. These results suggest that both calcium-dependent and calcium-independent signaling pathways drive CXCR3-A-mediated cell migration. In addition, our data support the possibility that ERK, p38, or Akt may mediate the calcium-independent pathways.
In contrast to results obtained with CXCR3-A, our data indicate that CXCR3-B, which does not induce chemotaxis, also does not affect [Ca2+]i or the p38 and PI 3-kinase/Akt signaling pathways.
It has been reported that I-TAC is a high-affinity ligand for the newly described chemokine receptor CXCR7 in some cells, including A549 cells (9). CXCR7 has been reported to promote cell growth and survival but, unlike other conventional chemokine receptors, does not affect cell movement or cytosolic calcium (9). This raises the possibility that I-TAC-induced responses were mediated by CXCR7 rather than CXCR3. However, we believe that our results are not mediated by CXCR7 for several reasons. First, our experiments in transfected A549 cells indicate that chemotaxis; changes in [Ca2+]i; and greater more sustained phosphorylation of ERK, p38, and Akt occur only in CXCR3-A transfectants and not in CXCR3-B or mock transfectants. The fact that I-TAC-mediated effects occur only in CXCR3-A-transfected cells tends to rule out an effect of CXCR7, since CXCR7 expression should be the same in all three transfectants. Second, IP-10, which does not activate CXCR7, produced robust chemotactic responses in CXCR3-A-transfected cells. Third, CXCR7 activation by I-TAC does not appear to increase phosphorylation of ERK or Akt (37).
The biological function of CXCR3 expressed by structural cells in the human lung is unclear. However, its ligands, IP-10/CXCL10, Mig/CXCL9, and I-TAC/CXCL11, are produced by airway and alveolar epithelial cells and are believed to play important roles in lung inflammation by selectively recruiting Th1/Tc1 lymphocytes, which highly express CXCR3 (4, 7, 36, 40). In fact, an inflammatory infiltrate comprised primarily of CXCR3-expressing Th1/Tc1 lymphocytes is present in several lung diseases in which CXCR3 ligands are overexpressed (e.g., COPD, sarcoidosis) (2, 35, 38). Of particular interest, in subjects with COPD, IP-10 expression is constitutively upregulated in whole lung homogenates and in small airway epithelial cells (21, 38). Moreover, CXCR3 knockout mice demonstrate greater bleomycin-induced pulmonary fibrosis than wild-type animals, suggesting that CXCR3 inhibits pulmonary fibrosis and remodeling, perhaps by affecting the behavior of lung structural cells (25). In addition, viral infection and the proinflammatory cytokines tumor necrosis factor-α, IL-1β, and IFN-γ increase production of the CXCR3 ligands (40, 44). Therefore, expression of CXCR3 by lung structural cells raises the possibility of autocrine or paracrine responses to CXCR3 ligands.
We have shown that CXCR3 induces directed cell movement in human pneumocytes. In airway epithelial cells, CXCR3 not only mediates chemotaxis but also induces DNA synthesis and cell proliferation (3). Because cell chemotaxis and proliferation are essential mechanisms in tissue repair (27, 29), the CXCR3 receptor expressed by human pneumocytes is likely to play a role in lung homeostasis and responses to injury.
In summary, the present study demonstrates that human alveolar type II pneumocytes constitutively express a functional CXCR3 receptor. In human pneumocytes, the CXCR3-A splice variant mediates chemotactic responses, increases cytosolic calcium, and activates ERK, p38, and PI 3-kinase/Akt kinases. The function of the CXCR3-B splice variant, whose mRNA is present in greater abundance, is unknown.
This work was supported by Temple University and the Philip Morris Foundation.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2008 the American Physiological Society


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Bursting at the seams with metaphors, themes, and symbolism, Alejandro González Iñárritu's Birdman teeters on the brink of becoming too busy for its own good. This is a film with a lot on its mind, and while it never delivers anything breathtakingly original, it explores interesting thematic material in mesmerizing fashion: cinematographer Emmanuel Lubezki (Gravity) shoots the film in a series of long continuous shots stitched together to give the effect that the movie is essentially one long take.
Director: Alejandro González Iñárritu
Starring: Michael Keaton, Edward Norton, Emma Stone, Amy Ryan, Naomi Watts
Michael Keaton plays Riggan Thomson, a mostly-forgotten actor famous for playing a superhero twenty years earlier - reminiscent of Keaton's real history with the Batman franchise. Two decades later, he's attempting to stage a comeback by writing, directing, and starring in a Broadway adaptation of a Raymond Carver short story. Thomson and his producer (Zach Galifianakis) have sunk most of Thomson's money into the play, so this is his last shot at regaining the cultural relevance he so desperately craves. Forced to replace a key cast member one day before previews begin, Thomson brings in Broadway wunderkind Mike Shiner (Edward Norton), an actor who constantly pushes the envelope to find the "truth" in his scenes. Pressure mounts as Thomson juggles a hectic schedule, a relationship with his just-out-of-rehab daughter (Emma Stone), his romantic entanglement with a co-star (Andrea Riseborough), the promise of a bad review from a theater critic, and his own insanity as he attempts to complete his journey of self-discovery.
Thomson's alter-ego - Thomson in a Birdman suit, speaking in a voice that parodies Christian Bale's guttural Dark Knight vocals - speaks to him throughout the film, representing the hauntingly easy option to return to the superhero suit and bank a huge paycheck. But Iñárritu is disgusted by blockbuster film culture, and while I certainly enjoy my fair share of superhero movies, this film takes a hard stance against them. Depicting superhero films as nothing more than empty spectacle and decrying the people who make them as purposely peddling filth to the masses, Birdman raises some strong (if well-worn) points, but its blanket generalizations are slightly troubling. The film presents its viewpoints as the definitive end-all be-all statement about superhero movie culture without leaving open the possibility that there could be any intelligence found in them at all. (Captain America: The Winter Soldier, a prescient film about the national surveillance state, comes to mind as an example from just this year that disproves this notion.)
Similarly, Birdman gets into some troubling territory with the confrontation between Thomson and a theater critic, falling into the classic "those who can't do, criticize" argument that any critic has likely heard dozens of times. For the record, the idea that someone becomes a film critic because they're a failed filmmaker is a fallacy; the art of criticism and the art of filmmaking are two separate things, and while an understanding of the process by which films are made is undeniably helpful in critiquing and analyzing the final product, a background as a director is not a requirement to discuss the merits and flaws in a piece of art. I understand the sentiments of not liking how blockbuster culture is permeating our society and thinking that critics are nothing more than people who sneer down their noses at those who take considerable creative chances, but to explore these topics in a way that leaves no room for discussion seems a bit misguided.
Thematically, Birdman covers some of the same ground as Damien Chazelle's excellent musical drama Whiplash, exploring ideas of legacy, relevance in the face of looming obscurity, and the sacrifices necessary to attain greatness in art. It explicitly equates love with human existence, and riffs on the concept of social media (which allows people to acknowledge one's existence) as an outlet for feeling fulfilled. The film, like the ever-moving camera, swoops from one theme to the next inside a claustrophobic theater, occasionally bursting through the front doors or onto the roof to capture a bit of New York City and a whole lot of Thomson's unstable mental condition (we see fireballs, giant robo-birds, and flight sequences through Thomson's unreliable eyes).
Keaton is great in the lead role, and Norton practically steals the film in one of the most fun supporting parts we've seen from him in years. The women don't fare as well because they aren't given as much to do (although Emma Stone's performance is a highlight), and even though there were a handful of elements I didn't particularly care for, Birdman is more than the sum of its parts. It's a dark, funny send-up of show biz that will hopefully send Michael Keaton soaring toward excellent roles again. Until next time...


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Current investment update
The United Kingdom Brexit Vote – how this is affecting investment markets
On Friday 24 June 2016, stock markets throughout the world fell between 3% to 8% due to the surprise Brexit vote regarding the United Kingdom's referendum on its future with the European Union (EU). The following provides a few brief comments on this issue.
The fall in the markets on Friday is primarily due to the surprise vote for the UK to leave the EU after more than 43 years of membership. Up until the vote, the markets had been factoring in a slight 'remain' victory – for UK's continuation within the EU – so the market reaction is no surprise given the shock outcome.
The markets most impacted were the pound, UK stocks and European stocks. Australian markets were the first to be affected given that our markets were operating when the result was finalised Friday mid-morning (Australian time). Later that day, as time zones caught up with the news, the selling continued in Europe and the US.
One source of the ongoing uncertainty relates to the process of 'divorcing' from Europe, with unknowns including the timing and ability for the government to negotiate an exit, and also putting in place new trade arrangements. This is further complicated by the resignation of the UK Prime Minister and expected changes to the government's key ministers.
Statewide suspects the market uncertainty will subside once these issues become more defined in the next few weeks. Sadly for the UK and Europe, the whole episode has weakened both entities and may possibly cause a recession in the UK. However, no one is sure until the new leadership and the path of exit becomes clearer.
In terms of portfolio positioning and strategy we have come into this environment with a slight defensive posture in holding more cash and absolute return strategies, which we believe will provide some buffer to the market volatility. There are no planned changes to our strategy other than seeking to take advantage of any market weakness by reducing our cash weight.
As always, we strongly believe that short-term forecasts should not drive investment decisions and we also believe that portfolio diversification across all asset classes should be at the core of our members' investment strategy.
It is important to remember that superannuation is a long-term investment and your timeframe in the market spans not only your working life, but your retirement also.
If you have any questions, or require any further information, please contact our client services team or Statewide Financial Planning on 1300 65 18 65.


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RICO By: Skylar Clark Racketeer Influenced and Corrupt Organization What Does "racketeering mean? (A) any act or threat involving murder, kidnapping, gambling, arson, robbery, bribery, extortion, dealing in obscene matter, or dealing in a controlled substance or listed chemical.
(B) any act which is indictable under any of the following provisions of title 18, United States Code: relating to bribery, sports bribery, counterfeiting, theft from interstate shipment, obscene matter, etc.. At first, RICO was meant to get rid of the mafia. In the 1980's, Congress realized that any civil claim to be brought by any person injured in their property is a RICO violation. If the person won the RICO claim, they would receive the amount of three times more then their actual damages and would be awarded their costs and attorneys' fees. This inspired everyone to try to have their civil claim fall under the RICO act. Because of RICO's broad function, it was easy for lawyers to portray their cases under the RICO act. RICO Law: What was the original intent? Basically, to get rid of the Mafia. Other groups added to the RICO act.. Hells Angels Key West PD Winter Hill Gang Major League Baseball Latin Kings What does "trusteeship" mean?!? "A person injured as a result of a RICO violation can recover treble damages and reasonable attorneys' fees. In order to prove a RICO violation, the person must be able to show that he or she was injured by a person associated with an "enterprise" that has been engaging in a "pattern of racketeering," which consists of at least two "predicate acts" during a ten-year period." (USLegal) 15 "Predicate Acts": 1. Secruity fraud 2. Mail fraud 3. Black Mail 4. Tampering with federal grand jury. 5. Obstruction 6. False Entry 7. Bank Fraud 7. Bank Fraud 8. Extortion 9. Wire Fraud 10. extortionate credit transactions 11. Obtaining of Property 12. Threats of Physical Violence I was a little confused on this question..all I could find about Jol Silversmith is how the 13th Amendment is missing?!? The 13th Amendment is the Emancipation Proclamation..so.. Reason 1 on Why they critcize RICO: It threatens business civil liberities Reason 2 on why they critcize Rico: Works Cited
-google.com/image The language of the act is too broad so it can involve cases involving malpractice Reason 3 on why they critcize RICO:
There is no criminal convictions are necessary to win a civil case under the act.
Reason 1:
RICO uses predicate acts that become apart of rackteering (muder, robbery, bribery, etc) Reason 2:
"When criminal organizations operate in several states, their offenses would normally have to be prosecuted separately in the states of federal judicial districts where the individual crimes occurred; however, by defining these offenses as part of a single pattern, the entire pattern can be prosecuted together as a single crime in any federal district where one of the predicate acts occurred. Procedural rules limiting the joinder of crimes or of defendants in a single indictment are inapplicable once the separate crimes or offenders are conceptualized as part of a single "racketeering enterprise" jointly committing the same crime." (RICO Effects)
Reason 3:
When the crimes are grouped and under RICO, the criminal gets a longer sentence. For example, a crime that would be a 10 year sentence would turn into a 35 year sentence under RICO. What I think about RICO.. I believe the longer sentences under RICO would deter criminals from committing crimes that could possibly fall under RICO. The only problem I see with RICO is that it is too broad.This could be bad for businesses with employees who claim something under RICO. But if you do the crime.. You gotta do the time.
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RICO-Criminal Law
Describing RICO
skylar clarkon 10 April 2011
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Relay For Life has kicked off 2010 with a flying start by celebrating a momentous milestone.
Warrnambool Relay For Life, now in its 8th year, recently announced their 2010 fundraising total of $145,000. This means they have raised more than $1 million for Cancer Council Victoria's cancer research, cancer support and cancer prevention programs.
Chairmanager Louise Richards was delighted with the outcome. "It is such a rewarding event to be involved with;over 1300 people attended the event. It's fantastic to see that support in the community. There are so many passionate people in the Warrnambool area who help grow the event year after year. "
"This milestone reflects the hard work by the dedicated volunteer organising committee, teams and the wider Warrnambool community." Ms Richards said.
With more than 25,000 Victorians diagnosed with cancer every year, Ms Richard said Relay For Life is a great way to fight back against cancer.
"We all know someone that has been affected by cancer whether they be a family member, friend or colleague." Ms Richards said. "Relay For Life is a great opportunity to tackle this fight together as a community and raise much needed funds."
There are over 40 events held across Victoria. To find your nearest event or for more information on Relay For Life visit, www.relayforlife.org.au.


text: Join Beautiful You charity shop as they celebrate Pink October with their third annual fashion show. Held at the Caloundra Rugby Union Club from 1.30pm to 4.30pm, ladies and gentlemen are invited to come along dressed to impress in their most fun, funky and fabulous attire. Guests are asked to bring a cup and saucer along to get into the spirit of the charity event. Prizes will be up for grabs for best dressed, best tie, best hat/fascinator and best cup and saucer, so bring your fashion A-game and a fun attitude for what's sure to be a great day for all. Tickets are $25 each, which includes coffee and tea, food, and of course, the fashion show.


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HS: Language and the Mind Prof. R. Hickey SS 2006 First and Second Language Acquisition. Tatiana Prozorova (HS/TN) Irina Novikava (HS/TN) Alexandra Wolek (HS/LN) Vanessa Hollands (HS/LN) Verena Scheulen (HS/LN) Nadiya Sowa (HS/LN) Kirsten Leicht (HS/TN). Overview.
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Tatiana Prozorova (HS/TN)Irina Novikava (HS/TN)
Alexandra Wolek (HS/LN)
Vanessa Hollands (HS/LN)
Verena Scheulen (HS/LN)
Nadiya Sowa (HS/LN)
Kirsten Leicht (HS/TN)
Tatiana Prozorova
Irina Novikava
Aleksandra Wolek (Hauptstudium LN)
Inherited attributes:
Sex, intelligence, personality and learning style
Social background:
Family structure, cultural environment, social group affiliation
Situation: setting, activity, number of participants
Child's linguistic behaviour
Style of linguisticinteraction: interpersonal relations etc.
no genetic superiority of girls
correlation between language and intelligence strongly related to environmental variation
no strong evidence for such relationship, still demands researching
all factors are very significant
for child's linguistic behaviour
relationship between experience of
linguistic interaction and patters of language learning is very complex
and variable
child's linguistic behaviour depends, for sure, on all these factors, however, the size and nature of this variation is unknown
Thank you for your attention!
Vanessa Hollands (Hs/LN)
Language acquisition does not take place in a vacuum. As children acquire language, theyacquire a sign system which bears important relationships to both cognitive and social aspects of their life.
Psychosocial aspects of language acquisition are
mainly concerned about how language, thought
and social interaction interrelate in the child's
Does social interaction influence the child's language acquisition?
Piaget focuses on the child's cognitive
development, which he describes as resulting
from the internalization of the means-ends
organization of the sensorimotor activity
achieved in early development.
He sees the children's use of language as one
among many behavoirs following principles of
organization and mechanisms of development
which are themselves autonomous .
autonomy and causal priority
cognitive development is in principle both autonomous from language development
and causal prior to it
The nature of children's language at any
particular time is explained as being merely one
of the many symptoms which reflect a
particular stage in their underlying cognitive
language as one phenomena among others, which can be explained in biological principles
The child's cognitive development is relatively
autonomous, not only independent from
language, but also from social interaction.
social interaction as secondary
social interaction explained in logico-
mathematical principles
The child's egocentricity results from his lack of
decentering. His language, having private
characteristics, is at first not adapted to social
communicative situations. It becomes socialized at a
later point in development as in decentering the child's
cognitive organization allows him to participate in social
child talks about what he does and is not
concerned about being understood
speech does not seem to have a real function
Vygotsky's approach to the inter-relations of
language, thought and social interaction is to
view language as a multifunctional and context-
dependent system mediating simultaneously
cognitive and social development.
Vygotsky defines language as primary, context-
dependent and social natured.
Language development is the principal motor of
development, as it mediates the child's participation in
both the intellectual and social life surrounding him.
cognitive development is not independent from signs
He sees a constant interaction between
language development and cognitive
development, such that thought is neither
autonomous from language nor causally prior
To it.
The use of a sign system such as language are
necessary for the development of uniquely
higher mental functions.
The cognitive development is necessary
dependent on the fact that language is
The context-dependent indicatory aspects of
communication in social interaction are primary and
constitute the foundation for the development of
abstract reference-and-predication.
Zone of proximal development
It can be generally described in terms of the
processes of social interaction between adults
and children which allow children to organize
complex series of actions in problem-solving
situations before they have the mental
capacities to decide on the actions on their
shift from interpsychological to intrapsychological
How does this shift in function take place?
At first, speech accompanies ongoing actions in the context of utterance, serving as a means of social contact with others. At a later point, when speech has been differentiated it forms a system which is multifunctional for the adult:
change in different functions
Contrast between Piaget and Vygotsky:
Thanks for your attention!
Verena ScheulenHauptstudium LN
… in everyday communication
"And then he put it in his knee."
"He put it on his knee?"
Nadiya Sowa (Hauptstudium LN)
Example: The man whom I spoke to him is a teacher
Example: Chinese and Japanese languages don't contain relative clauses
Example: Chinese learners tend to overuse expressions of regret in English, because of norms of their mother tongue
Example: My brother made me to give him some money.
Example: "no+verb" –negatives to perform statements
"don't+verb" – negatives to perform commands
multidimensional model
Example: Gestern ich gehe ins Kino. (Yesterday I go to the cinema.)
Gestern gehe ich ins Kino. (Yesterday go I to the cinema.)
socio-psychological factors
Kirsten LeichtTN Hauptstudium
mieten-vermieten rent-let
kaufen-verkaufen buy-sell
one should resist to translate piece by piece
She is interested in philosophy. vs. The philosophy of Kant.
Hose – trousers, Schere – scissors, die Möbel – furniture
e.g. on foot – zu Fuss, by train – mit dem Zug
to fill in – ausfüllen
to stand out - auffallen
follow a verb
e.g. He wants her to sing a song. (infinitive complement)
Er will, dass sie ein Lied singt. (causal complement)
He saw him running away. (participle construction)
Er sah ihn weglaufen. (infinitive complement)
e.g. They gave him the book. - He was given the book.
i.o. d.o.
Sie gaben ihm das Buch. - Er wurde das Buch gegeben.
In German this is strictly forbidden.
e.g. Er ist Freitag abgereist. – He departed on Friday.
1980 ist er nach München gezogen. – He moved to Munich in 1980.
- prepositional distinctions; e.g. in time: rechtzeitig, on time: zur rechten Zeit
e.g. aktuell 'topical' actual 'tatsächlich'
dumm 'stupid' dumb 'stumm'
Gift 'poison' gift 'Geschenk'
sensibel 'sensitive' 'sensible' 'vernünftig'
glücklich happy, lucky
seit for, since
dress Kleidung, Kleid
go gehen, fahren
A crowning achievment. Eine Spitzenleistung
Der krönende Abschluss. The final flourish.
Ein preisgekröntes Buch. An award-winning book.
A crowning achievment. Eine Spitzenleistung
Der krönende Abschluss. The final flourish.
Ein preisgekröntes Buch. An award-winning book.
dictionaries don't provide enough information on the usage of the words
e.g. Zwei Fliegen mit einer Klappe schlagen
To kill two birds with one stone.
die Daumen drücken
keep your fingers crossed
ganz Ohr sein
to be all ears
Eulen nach Athen tragen
to bring coals to Newcastle
e.g. leagle eagle – Staranwalt Kind und Kegel
shop till you drop über Stock und Stein,…


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Russian Photographer, (20th century). Russian. Medium: black and white photograph. Date: 19th Century. Michael (1832-1909) was the 7th child of Tsar Nicholas I of Russia and Charlotte of Prussia; Provenance: Private Collection. Photographic Rights held by The Bridgeman Art Library.
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Armed with gift cards and a zeal for bargains, crowds returned to the nation's malls and stores Monday for a second round of holiday shopping...
NEW YORK — Armed with gift cards and a zeal for bargains, crowds returned to the nation's malls and stores Monday for a second round of holiday shopping as retailers hoped for a post-Christmas sales blitz.
Some retailers already know it's been a good season. Seattle-based online giant Amazon.com said its holiday sales worldwide set a record this year, powered by strong demand for Apple Computer's iPod music players, video games and jewelry.
But many stores — stymied by shoppers procrastinating more than usual — are relying heavily on the post-holiday business to meet their modest sales goals. They wooed customers with deeper discounts, expanded shopping hours and fresh regular-price merchandise.
They're largely aiming their efforts at the growing numbers of gift-card holders who are expected to spend their newfound money. Gift cards are recorded as sales only when they're redeemed.
"Retailers have recognized that December has 31 days," said Marshal Cohen, chief analyst at NPD Group, a market-research firm based in Port Washington, N.Y.
In fact, a growing number of stores such as Coach, Target and American Eagle Outfitters rolled out some spring merchandise, while KB Toys pushed new versions of Barbie and the funky Bratz dolls.
Consumer-electronics chains such as Best Buy highlighted CDs, DVDs and video games in their advertising, counting on shoppers to feed the gadgets they received as gifts.
Online sites such as overstock.com and buy.com courted customers with free shipping deals and deeper discounts Monday, though online shopping has been a bright spot in the season.
At Amazon, shoppers bought more than 108 million items between Nov. 1 and Christmas, the online retailer said Monday, without providing revenue figures. The busiest day was Dec. 12, when customers ordered 3.6 million items.
Amazon this year introduced an online-gift organizer that allows users to build a list of the people they give presents to on Christmas and other holidays. The site also offered shopping guides from more than 40 magazines including Bon Appétit, Cosmopolitan, Esquire and Lucky.
Amazon said it sold a $94,000 pair of diamond earrings during the holidays. The most popular video games were "Mario Party 7" for Gamecube and Sid Meier's "Civilization IV" for personal computers, the company said.
Different models of iPods were Amazon's top three hottest sellers in electronics.
Gifts set in ink
Most shoppers braving Monday's crowds were clamoring for a deal.
Plan A for the day after Christmas in Seattle was new tattoos, a gift Teddy Taylor gave his wife, Lisa.
When they found the tattoo parlor wasn't open yet, they settled for Plan B: joining the throngs of shoppers at Seattle's Westlake Center making the switch from buying for others to buying for themselves.
The Taylors bought a teapot and some books.
A sign at Macy's read "To: me, From: me." Another, at Gap, promised "instant gratification — Use your Gap gift card."
One couple — self-described "poor college students" — put off exchanging gifts until Monday in hopes of finding deals. Some people were entertaining their out-of-town guests. Families were out together making returns and exchanging the gifts they got for the gifts they wanted.
Cheryl Kitashima of Mercer Island helped her 19-year-old daughter and niece.
"People were foolish enough to give them real presents instead of money," she said.
"Anything on sale"
Nationwide, the search for discounts brought millions out.
"We're looking for anything on sale," said Jennifer Westfall of Charleston, W.Va., who brought her mother and 7-year-old daughter to the local Charleston Mall. "Only cheapo markdowns."
Westfall found several deals, including a $130 cocktail dress for $20 and children's clothes discounted 90 percent.
Some shoppers were finishing their own Christmas shopping and some of the season's hottest gifts were sometimes in scarce supply. Kimberlee Wiley of New Bedford, Mass., went hunting for a $300 iPod digital music player Monday at the local Filene's department store, using all the gift cards she had received for Christmas. She discovered the iPods were sold out, and later bought one online.
While this week should be busy for retailers, Cohen of NPD expects that retailers will wind up with a modest sales increase of a little more than 3 percent for the November-
December period. The estimate is based on same-store sales, which are sales at stores open at least a year.
Michael P. Niemira, chief economist at the International Council of Shopping Centers, expects that 20 percent of gift-card holders will redeem their cards this week.
Seattle-based GiftCertificates.com said teens, the largest adopters of gift cards, are expected to redeem them an average of 30 days after receiving them.
According to ShopperTrak RCT, which tracks sales at more than 40,000 primarily mall-based stores, the week after Christmas accounted for 10 percent of holiday sales last year, but analysts expect that period to account for as much as 14 percent this year, given gift cards' soaring popularity.
The National Retail Federation estimates that consumers will spend $18.48 billion on gift cards this holiday season, up 6.6 percent from a year ago, based on a survey conducted by BIGresearch. But plenty of malls and stores are seeing larger increases.
Karen MacDonald, a spokeswoman at Taubman Centers, which operates or owns 23 malls in 11 states, reported that 25 percent of those redeeming gift cards on Monday were spending more than the value of the card.
Seattle Times staff reporters Emily Heffter and Monica Soto Ouchi contributed to this report, along with Associated Press writers Eric Tucker in Providence, R.I., Derrill Holly in Washington, D.C., and Larry Messina in Charleston, W.Va. Information about Amazon.com came from Bloomberg.


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Iron Maiden: London Shepherd's Bush Empire
Ver Maiden skirt along the thin line between 'sexy' and 'sexist'...
The touts are not happy. It's the second night of Iron Maiden's surprise two night residency at the Shepherds Bush Empire, and at 8.15 it's becoming clear that the expected walk-up of 'ironic' metal fashionistas and curious nu-metal teens has evaporated into the Sunday night drizzle.
Inside, however, all is denim'n'leather. Lead guitarist Dave Murray strolls on in shiny leather trousers and fires off a volley of what can only be called high octane riffola. Judging by the facial contortions which accompany it, this sends him into the uncharted hinterland between agony and ecstasy. He is swiftly joined by fellow lead guitarists Adrian Smith and Janick Gers (who, frankly, is David St. Hubbins), and the whole place is quickly gurning away in appreciation. So this is the heads-down mindless boogie that our ancestors told us about!
Bruce Dickinson sprints from the wings. Unlike the others, he is not togged out in the metal battle-dress of a thousand Donningtons, but in sweat-vest and shorts. Bruce knows he has a lot of hill-running to do. Not a song goes by without him clambering up the mountain of Marshall amps or teetering precariously on the stage-front monitors (when the others haven't already beaten him to it).
During a pulverising 'Two Minutes To Midnight' he bellows "So that's what you look like!" and you realise he's perched on the edge of the balcony whilst the band, giddy with joy, trade solos that would make Tap blush. The beyond-parody mood culminates in the arrival of ten-foot monster-mascot 'Eddie' who lurches on for the encores, during which the band reprise 'Number Of The Beast', first-ever single 'Sanctuary' (from 1980) and new, not dissimilar-sounding tune 'Out Of The Silent Planet'.
"We're off to raise some hell in South America!" yells Bruce at the close, as the band-crowd love-in concludes with a riot of devil-rock hand signals. An institution, and still mental.
Paul Moody


text:
MOVIE SYNOPSIS [ General Audiences ] Film of Matt Reynolds. Introduced in movie theaters in 2013, with a production coming from Czech Republic, Slovakia and USA. You can watch The Great Chicken Wing Hunt online on TV cable or theaters with original audio in English at different dates. This film premiered in theaters in 2013.
Rating: 5 by 32 users./
Runtime: 71 minutes
Ben Beavers, Al Caster, Freedom, Columbus Marshall Grady, Ric Kealoha, Lucie Mayerova, Matt Reynolds, Ron Wieszczyk and Dom Zanghi.
Documental, Adventure, Comedy.
71-minute film (full movie) directed by Matt Reynolds.
The original audio of The Great Chicken Wing Hunt has dialogues in Dolby Digital, it was produced in Czech Republic, Slovakia, USA.
It premiered in cinemas or television in 2013.
Robert Geile, Douglas Brantner and Eric Brouse.
Matt Reynolds, Elizabeth Mandel, Melinda Person, Drew Cerza, Chris Allingham, Larry Ann Evans and Alexander Roy.
Without commercial breaks, the full movie The Great Chicken Wing Hunt has a duration of 71 minutes; the official trailer can be watched in streaming on the Internet. You can watch this full movie free in EnglishDolby Digital in movie TV channels, renting the DVD or with VoD services (Video On Demand player, Hulu) and PPV (Pay Per View, Netflix).
See the page of this full movie, The Great Chicken Wing Hunt in FULLTV Movies.


text:
Life Cycle Nutrition: From Infancy to Adolescence. Chapter 15. Too few fruits, vegetables and whole grains Too many processed foods high in added sugar, salt, and processed fats Gets worse among adolescents. What are Children Eating in the US?. From NHANES, 2001-2002.
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Chapter 15
Too few fruits, vegetables and whole grains
Too many processed foods high in added sugar, salt, and processed fats
Gets worse among adolescentsWhat are Children Eating in the US?
From NHANES, 2001-2002
Total amount increases with age
Fat (%kcal)
Infants: 40-55%
1-3 yrs: 30-40%
4-18 yrs: 25-35%
Adults: 20-35%
Same percentage as adults (45-65%)
Fiber: 14g per 1000 kcals
Infants: soak 6-8 diapers daily
1-3: 1.3 L/d
4-8: 1.7 L/d
Needs increase with illness, high environmental temp, or PA
Variety of meats, legumes, eggs, whole grains, fruits, vegetables, and dairy (if appropriate)
Deficiency risks: Calcium, Iron, Vit. A & DNutrient Needs
TV exposes kids to food industry marketing
Takes the place of physical activity
Kids who watch 4 or more hours/day are 40% more likely to be overweight than those who watch an hour or less/day
Computer/video games also contribute to inactivityTelevision & Childhood Obesity
Saturday Morning Food Ads