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CHESTER, Pa., June 14, 2011 /PRNewswire/ -- Power Home Remodeling Group, the nation's fourth largest home improvement company, presented a $106,000 check to Alex's Lemonade Stand Foundation (ALSF) last Thursday, June 9 as part of a 15-hour CBS 3/CW Philly telethon called "A Stand for Hope: The Alex Scott Phone Bank." Power co-founder and president Adam Kaliner amended the check live on-air from $100,000 to $106,000 to help Alex's hit $1 million raised through the telethon. In total, $1,015,618 was raised, a record for the annual fundraiser which began in 2007.
ALSF is one of the leading foundations for pediatric cancer, raising more than $40 million and funding more than 200 cutting-edge research projects. This donation is the first since Power's commitment earlier this year to donate one dollar per window or per square foot of siding or roofing installed throughout the year in an effort to raise awareness of pediatric cancer among local communities. In 2010, Power installed energy saving and environmentally friendly solutions to more than 14,000 homes and is on track to donate at least $300,000 to ALSF in 2011.
"This partnership is an important extension of Power's commitment to our community," explained co-founder and president Adam Kaliner. "We're bringing Alex's courageous story into the homes of our customers up and down the east coast in an effort to grow support for the foundation in new communities. We are excited to make this initial contribution as a testament to our commitment to this important foundation — with a promise for more to come throughout the year."
Power hosted an Alex's Lemonade Stand at each of its five regional offices over the past week in celebration of national Lemonade Days (June 10-12) where volunteers from across the country took a united stand against pediatric cancer by holding fundraisers of their own. So far, the company has raised another $3,050 through these stands. The company also encouraged its 900 employees to support Alex's by hosting lemonade stands at home.
Power is also hosting the first ever "Power Run" for ALSF, scheduled to take place in October in Media, Pa., becoming an annual company tradition. Power will further support Alex's by donating $100 for each customer referral that selects a "donation reward" throughout the year.
Additionally, Jeff Kaliner, co-founder and chief executive officer of Power will join ALSF's 11 existing Board Members in an effort to help the foundation grow and succeed in fulfilling Alex's vision of finding a cure for childhood cancer. As a new Board Member, Kaliner recognizes the importance of staying true to Alex's front yard beginnings and is committed to serving the foundation's mission in the spirit of children who remain optimistic and caring throughout their battle with cancer.
"We were thrilled to have Power Home Remodeling Group come on board as a sponsor of Alex's Lemonade Stand Foundation in 2011," says Liz Scott, Alex's mom. "Their commitment to helping achieve Alex's quest for a cure has only become more evident as the year has progressed, both through their recent donation at the Phone Bank, and Jeff's addition to our Board of Directors. We continue to be amazed by the dedication of this group."
Jeff Kaliner added, "I'm honored to join this prestigious Board of Directors of like-minded individuals who share an interest in promoting one little girl's remarkable vision. I'm thrilled at the opportunity to further support the children served by Alex's and am confident in Power's ability to make significant contributions moving forward."
For more information about Power's partnership with ALSF – or how to host your own Alex's Lemonade Stand – please visit AlexsLemonade.org.
About Power Home Remodeling Group
Family-owned since 1992, Power Home Remodeling Group is the nation's fourth largest home remodeling company with more than 900 employees and $135 million in sales. Headquartered in Chester, Pa., Power provides energy-saving and environmentally friendly exterior remodeling solutions to residents on the East Coast, including Connecticut, Delaware, Massachusetts,
Maryland, New Jersey, New York, Pennsylvania, Virginia, and Washington, DC. An Inc. 5000 company, Power has served more than 50,000 homeowners and is recognized as a home improvement leader by its 2009 "Dealer of the Year" award from Window and Door Magazine and the 2010 and 2011 "Top Workplace" from The Philadelphia Inquirer. For more information, please visit PowerHRG.com.
About Alex's Lemonade Stand Foundation
Alex's Lemonade Stand Foundation emerged from the front yard lemonade stand of cancer patient Alexandra "Alex" Scott (1996-2004). At the age of 4, Alex announced that she wanted to hold a lemonade stand to raise money to help find a cure for all children with cancer. Since Alex held that first stand, the Foundation bearing her name has evolved into a national fundraising movement, complete with thousands of volunteers across the country carrying on her legacy of hope. To date, Alex's Lemonade Stand Foundation, a registered 501(c)3 charity, has raised more than $40 million toward fulfilling Alex's dream of finding a cure, funding over 200 research projects nationally. For more information visit www.AlexsLemonade.org.
SOURCE Power Home Remodeling Group


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On Tuesday January 8th, 2013 I appeared on a webinar at Moviola.com hosted by Michael Horton of the Los Angeles Creative Pro User Group.
The web broadcast was free to watch live. The webinar is available for download on demand for $15.
Download the on-demand webinar to see me change the default settings for built-in Final Cut Pro X effects, bring the additional effects available in Motion 5 into Final Cut, and combine Motion’s advanced controls into single Final Cut Pro X effect controls.
The final effect that I make in the webinar corrects the kind of fish-eye distortion that some wide angle lenses can add to footage. I show how it corrects narrow, medium and wide angle GoPro footage.
The download includes:
– The hour+ webinar
– The footage I used in a Final Cut Pro event
– The timeline I used in a Final Cut Pro project
– The new effects created in Motion which you can immediately use in Final Cut
– My script, on which I based my completely ad-libbed presentation:
If you follow along, you’ll have made new effects you can immediately use in your editing projects.
All the Final Cut Pro X effects, transitions, titles and generators I’ve made available for free on this blog were made using Motion 5.
The webinar is an introduction on how Motion 5 works with Final Cut. It will start you on a journey towards making effects to save you time on your own projects and tools you can share with the rest of the Final Cut Pro X world.
Here are some comments from those who attended the live webinar:
“Cracking insight.” – Seth H.
“Listening from Wexford ireland – you have saved me a ton of time. Thanks Alex!”– Christian O.
“Very useful, great presentation.” – Artesia A.
“Thank you. Great webinar and thanks for your time.” – Ray B.
“Just a quick note, this is brilliant!” -Jim M.
“Just wanted to thank Alex for all his hard work, filters, blog, shares etc.” – Snow R.

domain: hobby


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Manufacturing, Engineering & Energy News Channel
19-11-2013A Cold alarm is essential for safety this winter image
19-11-2013Boston Limited unveil latest Viridis Microserver powered by the ARM® A15-based Calxeda EnergyCore™...
19-11-2013Brilliant Harvest installs Solar Panel System for Wyke Farms as cheesemaker goes 100% Gree... image
19-11-2013Electrical Installation? Trade Skills 4U Wrote the Book on That!
19-11-2013Underscore announce the rebrand of the UK's financial capability charity.
18-11-2013UK company sends safe drinking water equipment to typhoon-struck Philippines
18-11-2013Blue Coat Empowers Business with New Advanced Threat Protection Solution
18-11-2013OIL AND GAS – SMALLER OPERATORS ARE THE WINNERS IN THE TALENT WAR Super majors...
18-11-2013British LED technology company launches the first whole home, circadian, consumer smartbul... image
14-11-2013Darren Watkins joins Virtus Data Centres as new Sales Director
14-11-2013Nissan Selects Steelwedge to Support its European Sales and Operations Planning Processes
13-11-2013Mezzanine International Moves to the Next Level
13-11-2013BIOS IT launches ultra-fast server solution for high frequency trading at Low Latency Summit New Y...
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12-11-2013Eniram expands its international operations to Japan image
12-11-2013Eniram expands by opening new office in Germany image
12-11-2013Mayflex Develop IP CCTV Courses
07-11-2013CAST Sees Accelerated Growth and Rising Demand
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06-11-2013One of the UK's largest Solar Panel systems, built for Asset International by Brillian... image
05-11-2013New Allot solution provides the functionality recently demanded by the Coalition to protect childr...
04-11-2013Global Investment and Fund Administration Firm moves Risk Management to the Cloud
04-11-2013Advanced 365 launches Wi-Fi application enabling Mitsubishi Electric customers to control air-cond...
01-11-2013Pre-formed silicone sponge tubes from SFS offer neat, efficient, high-temperature insulati... image
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31-10-2013Smart UK Project searches for the UK's most innovative mobile companies image
31-10-2013CIBSE shows that non-compliance with Energy Performance of Building Regulations is costing million...
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29-10-2013Vent-Axia's Lo-Carbon Energy Saving Fan Triumphs at Top Industry Awards image
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28-10-2013Nationwide Selects WaterCoolersDirect.com for Drinking Water Solutions WCD Wins Contract t... image
24-10-2013Southern Manufacturing Show 2014 on track for record year
23-10-2013Anderman Ceramics Ltd. successfully exhibited at the annual Glassman America 2013, Las Veg... image
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22-10-2013Eniram to attend Kormarine 2013 with Hyundai e-Marine and WorldOcean
22-10-2013STYROFOAM and XENERGY BIM objects launched image
22-10-2013Will Labour's energy price freezes put the lights out?
18-10-2013Top management changes at TMD Technologies
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15-10-2013EU BIDDING PROCESS NEEDS REFORM, SAYS EFFICIO

domain: news


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Recently Added Videos
Alexandru Tomescu Performance
Moonshine Society Performance
The Voice of Anne Frank Performance
Eishin Nose's The Gate Performance
Brandon Camphor & OneWay
Singer, songwriter, and producer Brandon Camphor leads the DC area Christian band OneWay—singers Angela Jones, Jayna Cullens, and Fred Cleveland and musicians Joshua Davies (keys), Jerome Baylor (drums), Myron Mollon (guitar), and Larry Mack (bass).
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domain: artistic


Role of Standing-Wave Mode Structure in Microlaser Emission
We have developed the first working microlaser, a laser oscillator in which coherent light is generated by means of the interaction of a single, excited two-level atom with a single mode of the radiation field. i In this experiment, inverted two-level atoms in an atomic beam traversing an ultrahigh Q optical resonator interact with the cavity mode one by one, and emit photons into the resonator. Because of the long cavity storage time, a large number of photons can build up. In this device the photon generation process follows the Jaynes-Cummings model, and the emission process is significantly different from that of conventional lasers. Photon build up is initiated by vacuum Rabi oscillations, not by spontaneous emission as in conventional lasers. Furthermore, amplification of the field is accomplished by the quantized Rabi oscillation process, and under appropriate conditions highly nonclassical photon distributions can be generated, such as photon-number trapped states.’ The microlaser is the optical analog of the micromaser,3 which operates in the microwave regime. However, operation in the optical range provides new experimental opportunities associated with the large increases in photon energy and momentum. The increase in photon energy allows measurement of the microlaser mean photon number and emission spectrum 4 via direct photon detection, whereas only atoms can be probed in the micromaser. The increased photon momentum should make it possible to study the entanglement of the quantized Rabi oscillations with the mechanical degrees of freedom of the atom, as exchange of a single optical photon with the cavity field can significantly deflect the atomic trajectory.5 In addition, the absence of blackbody radiation at optical frequencies opens the possibility of studying the features of quantum collapse and revival,6 which are entirely due to the superposition of discrete photon-number Fock states in the cavity field. Also promising is the possibility of generating and studying photon-number trapped states.
KeywordsCavity Mode Photon Number Blackbody Radiation Cavity Field Rabi Oscillation
- 4.S. Qamar and M. S. Zubairy, Phys. Rev. A 44, 7804 (1991); M. O. Scully et. al., ibid. 44, 5992 (1991); T. Quang et. al., ibid. 48, 803 (1993); K. Vogel et. al., ibid. 48, 813 (1993).Google Scholar
- 5.M. J. Holland, D. F. Walls, and P. Zoller, Phys. Rev. Lett. 67, 1716 (1991); A. B. Matsko et. al., Phys. Lett. 192, 175 (1994).Google Scholar
- 8.K. An and M. S. Feld, Phys. Rev. A, in press (August, 1995).Google Scholar


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2 killed and 10 more injured as vehicle strikes crowd near mosque in London
At least 2 people were killed and eight others wounded on Monday after a van mowed down worshippers leaving a mosque in London’s Finsbury Park. One person has been arrested so far after the incident at Seven Sisters Road. The driver, 48, of the van was first detained by the members of the public, then arrested by the police. After describing it as a “major incident”, the police are currently investigating if it was an act of terror. British Prime Minister Theresa May has informed that the incident is being treated as a potential terrorist attack by the police. She is also going to chair an emergency response meeting later in the morning.
After commending the emergency services, London Mayor Sadiq Khan said, “I have been in contact with the Met Commissioner and senior officers and am being kept updated on all developments. I have also spoken with community organisations in the area, local MP Jeremy Corbyn and leader of the council Richard Watts.”
Reacting to the incident, the Muslim Council of Britain (MCB), UK’ largest umbrella body, said on Twitter: “We have been informed that a van has run over worshippers as they left FinsburyPark Mosque. Our prayers are with the victims.”
The Metropolitan Police were called in just after 12:20 am (Local time) to the accident site on Seven Sisters Road, where van rammed into pedestrians. Many of the victims were leaving late night prayers after breaking their Ramadan fast.
One eyewitness, as cited by BBC, said, “There was this white van stopped outside Finsbury Park Mosque that seems to have hit people who were coming out of the mosque after prayers finished.”
The witnesses described the van swerving towards people, reported Guardian describing the nature of the collision.
London Ambulance Service tweeted: “We have sent a number of ambulance crews, advance paramedics and specialist responses teams to the scene.”

domain: politics


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Memory has always been the thing that brings me to photography over and over again. Being able to capture how I see a moment, or a person, or the light, or all of the above, keeps my mind bright and my shutter clicking. I earned my Bachelor's of Fine Arts in Photography from Emporia State University, and I am so pleased to be able to create and capture these gorgeous and personal moments for women.
— Alicia, Kansas City, KS
The best tips for what to do (and what to avoid) before and during your photoshoot!
We'll tell you the best tips on what to do (and not to do) before your shoot, where to shop, and how to make the best wardrobe choices for your body.


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Download E-books Cherry: A Life of Apsley Cherry-Garrard PDF
By Sara Wheeler
The 1st approved biography of the antarctic explorer who gave us the best vintage of polar literature
In February 1912, Apsley Cherry-Garrard drove a workforce of canine one hundred fifty miles to a desolate outpost on Antarctica’s tough ice shelf to fulfill Robert Falcon Scott and his males, who have been anticipated to come back victor-ious any day from their epic race to the South Pole. iciness used to be last in, and Cherry used to be handicapped by means of brutal temperatures and diminishing mild. below weeks later, 3 death males pitched their tent for the final time simply twelve miles to the south. One used to be Captain Scott, the chief of the day trip. the opposite , Birdie Bowers and invoice Wilson, have been the nearest pals Cherry had ever had.
Ten months later, as soon as the polar iciness had published them from captivity, Cherry and his seek occasion came across the tent, piled with snow and pinned to the ice by means of his buddies’ corpses. It used to be a tragedy that will rever-berate around the globe and encourage Cherry to put in writing his masterpiece, The Worst trip within the World, which lately crowned National Geographic’s record of the a hundred maximum event books of all time.
Cherry came across in his writing a way to see his grief and anger, yet in existence those doubts and fears proved a long way tougher to quell. because the years stepped forward, he struggled opposed to melancholy, breakdown, and depression, and was once haunted by way of the chance that he on my own had had the chance to avoid wasting Scott and his pals.
Sara Wheeler’s Cherry is the 1st biography of this soul-searching explorer, written with unrestricted entry to his papers and the total cooperation of his widow—who has refused all requests earlier. Wheeler’s biography brings to lifestyles this nice hero of Antarctic exploration and provides us a glimpse of the bad human price of his adventures.
Read Online or Download Cherry: A Life of Apsley Cherry-Garrard PDF
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Additional resources for Cherry: A Life of Apsley Cherry-Garrard
Extra importantly, for his internal existence a minimum of, he have been immensely gratified via the luck of The Worst trip on the earth following its first booklet in 1922. He used to be thirty-six while it got here out, and he acknowledged later that it was once a sequel to the friendship that had existed among him, invoice and Birdie. The publication had taken decades to accomplish, and as he pored over the pages within the quiet library, his head diminished over his father’s table, he heard back the long-silenced voices calling out around the ice, and glimpsed the normal smiles he had enjoyed see you later in the past. As he brooded, he appeared again at his vanished self, and while he took up his pen once again his stressed mirrored image seeped into his prose. a lot of The Worst trip is infused with a specific, plangent nostalgia. A iciness trip to Cape Crozier lay on the center of his e-book, and as he grew older it took on an iconic function in his lifestyles. in the course of their first iciness at the ice, Cherry, invoice and Birdie had got down to acquire the eggs of the Emperor penguin, incubated, by myself within the wildlife, throughout the Antarctic darkness. on the time, it used to be generally believed that if tested at an early level of improvement, Emperor embryos may yield an extraordinary Darwinian prize: they might demonstrate the hyperlink among birds and reptiles. the adventure to fetch the eggs took 5 weeks: the temperature fell to minus seventy five levels Fahrenheit, the tent blew away and the men’s necks iced up the instant they bent to drag their sledges. Then their enamel shattered within the chilly. but, Cherry wrote, ‘We didn't overlook the Please and thanks . . . And we saved our tempers, regardless of God. ’ in simple terms seven months later invoice and Birdie perished at the nice Ice Barrier with Scott, and whilst Cherry eventually received the valuable eggs domestic the employees on the normal background Museum made him wait in a hall, then became up their noses. The eggs turned the critical image of Cherry’s parable. ‘If you march your wintry weather Journeys,’ he wrote on the finish of his epic, ‘you could have your gift, as long as all you will want is a penguin’s egg. ’ He had concept his manner past crampons and rations and snow-blindness, and entered the immortal sector. For a time it seemed that the method of writing his Antarctic tale had quietened his anxieties: one of those cathartic redemption. There were chuffed months and years while the home was once packed with the controversy of kids. Girlfriends had come and long past; new friendships have been cast. yet because the years unravelled, a number of the versions of The Worst trip coated up at the glazed bookshelves couldn't assuage Cherry’s guilt and self-recrimination. The truths he had captured in his paintings have been tougher to discover off the web page. He was once born, on 2 January 1886, at 15 Lansdowne highway, a indifferent, red-brick residence on a tree-lined street in deeply first rate Bedford. there has been not anything ornate concerning the homes on the street: they have been designed for giant, middle-class households with extra aspirations than money. His father, Colonel Apsley Cherry, was once fifty-three, the second one son of a wealthy relatives of attorneys and civil servants who had settled in Berkshire a iteration ahead of him; his mom, Evelyn Sharpin, used to be twenty-eight, the daughter of an eminent Bedford health professional.

domain: library


text:
Edna St. Vincent Millay
I had forgotten how the frogs must sound
After a year of silence, else I think
I should not so have ventured forth alone
At dusk upon this unfrequented road.
I am waylaid by Beauty. Who will walk
Between me and the crying of the frogs?
Oh, savage Beauty, suffer me to pass,
That am a timid woman, on her way
From one house to another!
Edna St. Vincent Millay's Other Poems
Read this poem in other languages
This poem has not been translated into any other language yet.
Comments about this poem (Assault by Edna St. Vincent Millay )
The Road Not Taken
If You Forget Me
Still I Rise
Edgar Allan Poe
I Know Why The Caged Bird Sings
Stopping by Woods on a Snowy Evening
William Ernest Henley
Did you read them?
- A Soldiers Lament, Phil Soar
- The Sloth, Phil Soar
- The Double Play, Robert Wallace
- Kippers, Phil Soar
- what does hope tell you?, RIC S. BASTASA
- OUT, Phil Soar
- then we have changed from quizzical to a.., RIC S. BASTASA
- A Fishy Tale, Phil Soar
- those who are dying, RIC S. BASTASA
- For Lou and the rest of us, RIC S. BASTASA


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Liver inflammation and injury are mediated by the innate immune response, which is regulated by Toll-like receptors (TLR). Activation of TLR9 induces Type I interferons (IFNs) via the interferon regulatory factor (IRF)-7. We investigated the roles of Type I IFNs in TLR9-associated liver injury in mice.
Liver injury was induced in wild-type (WT), IRF7-deficient, and IFN-α/s receptor-1 (IFNAR1)-deficient mice by administration of ligands for TLR9 or TLR2. Findings from mice were verified in cultured hepatocytes and liver mononuclear cells, and in vivo experiments using recombinant Type-I IFN and interleukin-1 receptor antagonist (IL-1ra).
Type I IFNs were upregulated during TLR9-associated liver injury in WT mice. IRF7- and IFNAR1-deficient mice, which have disruptions in Type I IFN production or signaling, respectively, had greater amounts of liver damage and inflammation, decreased recruitment of dendritic cells, and increased production of TNF-α by liver mononuclear cells (LMNC). These findings indicate that Type I IFNs have anti-inflammatory activities in liver. The IL-1ra, which is produced by LMNC and hepatocytes, is an IFN-regulated antagonist of the pro-inflammatory cytokine IL-1β; IRF7- and IFNAR1-deficient mice had decreased levels of IL-1ra, compared with WT mice. IL-1ra protected cultured hepatocytes from IL-1β-mediated sensitization to cytotoxicity from TNF-α. In vivo exposure to Type I IFN, which induced IL-1ra, or administration of IL-1ra reduced TLR9-associated liver injury; the protective effect of Type-I IFNs therefore appears to be mediated by IFN-dependent induction of IL-1ra.
Type I IFNs have anti-inflammatory effects mediated by endogenous IL-1ra which regulates the extent of TLR9-induced liver damage. Type I interferon signaling is therefore required for protection from immune-mediated liver injury.
Liver-related etiologies are among the top ten leading causes of death in the United States.1 The common hallmark of most liver diseases is inflammation and injury, which may result in acute liver failure, or, if persist, promote the development of fibrosis and eventually cirrhosis.2 Presently, liver inflammation and injury have no pathogenesis-specific treatment, but they share a common pathway of induction of innate immune responses, triggered by Toll-like receptors (TLRs).3
For example, TLR9 is activated by unmethylated DNA rich in cytidine-phosphate-guanosine (CpG). This motif is present in bacterial DNA and also in DNA from apoptotic mammalian cells.4 Emerging data provide evidence for the role of CpG DNA and TLR9-mediated inflammation in acute and chronic liver injury of diverse origin, including alcoholic liver disease,5 primary biliary cirrhosis,6 primary sclerosing cholangitis7 and acetaminophen-induced liver injury.8 TLR9-initiated signals are also involved in general processes such as liver fibrosis,9, 10 liver cirrhosis,11 ischemia-reperfusion injury,12 and liver graft rejection13. TLR9 acts synergistically with the TLR2 ligand lipoteichoic acid (LTA),14 and further sensitizes the liver to injury induced by the TLR4 ligand lipopolysaccharide (LPS).15, 16
Activation of TLR9 by CpG results in increased production of inflammatory mediators via the nuclear factor κB (NFκB), and in a strong induction of Type I interferons (IFN-α and IFN-β) via the interferon regulatory factor 7 (IRF-7),17 which together with IRF3 also plays a role in TLR4-dependent induction of Type I IFNs. 18 While NFκB-dependent induction of inflammatory cytokines by CpG is considered the key event in the TLR9-mediated liver injury,5, 6, 8, 13 little is known about the role of IRF7-dependent Type-I IFN induction and signaling after TLR9 stimulation.
Here we demonstrate that induction of Type I IFNs and Type I IFN-mediated signaling has a protective role in TLR9-induced liver inflammation and injury. We report that impaired induction of interferon-stimulated genes, including the anti-inflammatory cytokine, interleukin 1 receptor antagonist (IL-1ra), increases liver inflammation and injury. Our results also demonstrate a protective effect of the IL-1ra in vivo in TLR9-associated liver injury.
The B6.129F2 and C57Bl/6 wild-type (WT) mice were purchased from Jackson Laboratory. IRF7-deficient (IRF7-/-) mice on B6.129F2 background were provided by Tadagatsu Tanaguichi (Tokyo) and type I interferon α/β receptor 1-deficient (IFNAR1−/−) mice on the C57Bl/6 background were the kind gift of Jonathan Sprent (Scripps Research Institute, La Jolla, CA). All animals (3–6/experimental group) were 6–8 weeks old and received proper care in agreement with animal protocols approved by the Institutional Animal Use and Care Committee of the University of Massachusetts Medical School.
We employed a previously described model of TLR9-associated liver injury induced by administration of TLR9 and TLR2 ligands.15, 16 After acclimatization, WT, IRF7−/− and IFNAR1−/− mice were injected intraperitoneally (i.p.) with saline or the combination of 2.5 mg/kg unmethylated DNA rich in cytidine-phosphate-guanosine (CpG, ODN1826 murine TLR9 ligand; InvivoGen, San Diego, CA), and 5 mg/kg lipoteichoic acid (LTA, from Staphylococcus aureus; Sigma, Saint Louis, MO). Three days after the above priming stimulus, the mice were injected i.p. with either saline or 0.5 mg/kg lipopolysaccharide (LPS, from Escherichia coli 0111:B4, Sigma, St. Louis, MO) and sacrificed as indicated. Some C57Bl/6 WT mice received a single i.p. injection of 100,000 IU human pegylated interferon alpha-2b (pegIFNα2, Pegintron, Schering, Kenilworth, NJ) two hours prior to LPS. Others were pretreated with recombinant human interleukin-1 receptor antagonist (IL-1ra) 25 mg/kg i.p. every six hours (Anakinra, Amgen, Thousand Oaks, CA) for 24 hours before CpG+LTA, and the treatment with IL-1ra was ongoing until sacrifice. Serum was separated by centrifugation. Livers were snap frozen, stored in RNAlater (Qiagen GmbH, Hilden, Germany) or fixed in 10% neutral-buffered formalin. ALT was quantified by biochemical assay (D-Tek Analytical Laboratories Inc, San Diego, CA).
Sections of formalin-fixed, paraffin-embedded livers were stained with hematoxylin and eosin (H&E), and assessed for inflammatory infiltrate; area of inflammatory infiltrates was calculated with Microsuite (Olympus Soft Imaging Solution GmbH, Munster, Germany) image analysis software in 20 high power fields.
Animals received anesthesia with ketamine (100 mg/kg) and xylazine (10 mg/kg); the livers were perfused with saline solution followed by in vivo digestion, as we previously described.19 The hepatocytes and liver mononuclear cells (LMNCs) were purified by centrifugation at slow speed (500g) and in Percoll gradient, respectively.
Cells were washed in PBS and incubated with anti-CD68 (FITC), anti-CD11c (FITC) or anti-PDCA1 (Alexa Fluor 647) antibodies for 30 minutes on ice. After incubation, cells were washed with PBS, fixed in paraformaldehyde and analyzed by flow cytometry. All antibodies were from eBioscience (eBioscience, Inc., San Diego, CA).
Primary hepatocytes were cultured in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal bovine serum (FBS), 1% insulin, transferrin, and selenium supplement on collagen-coated plates (Becton Dickinson Labware, Bedford, MA). Primary LMNCs were cultured in DMEM with 10% FBS. Hepatocytes were treated with recombinant murine IFN-α2b (500 IU/mL, eBioscience, San Diego, CA), murine IL-1ra (100 pg/mL, R&D Systems, Minneapolis, MN), murine IL-1β (100 IU/mL, Peprotech Inc., Rocky Hill, NJ) or murine TNF-α (0-100 ng/mL, Peprotech Inc., Rocky Hill, NJ). LMNCs were treated with mouse IFN-α2b or LPS (100 ng/mL, Sigma, St. Louis, MO).
Lactate dehydrogenase (LDH) release from the hepatocyte into the culture supernatants was measured using the LDH-cytotoxicity assay kit (Abcam, Cambridge, MA), and normalized to total LDH (determined after treatment of cells with detergent-based lysis solution).
Serum concentrations of the secreted forms of interleukin-1β (IL-1β) and IL-1 receptor antagonist (IL-1ra) were analyzed with ELISA (R&D Systems, Minneapolis, MN). Monocyte chemotactic protein 1 (MCP-1) in the liver lysate was measured with ELISA from R&D, and TNF-α in cell culture supernatants was analysed using ELISA from BD Biosciences (BD Biosciences, San Jose, CA).
RNA was extracted from liver tissue using the RNeasy kit (Qiagen Sciences, Maryland, USA) and on-column DNase digestion was performed using the DNase Set (Qiagen GmbH, Hilden, Germany); cDNA was synthesized with Reverse Transcription System (Promega Corp., Madison, WI). Real-time quantitative polymerase chain reaction (qPCR) was performed using the iCycler iQ Cycler (Bio-Rad Laboratories, Inc., Hercules, CA) and specific primers (Supplementary Table 1).
The data are presented as mean ± SEM. Comparison of the means was performed using Student’s T-test or Kruskall-Wallis test, when appropriate. P values less than 0.05 were considered significant.
TLR9 signaling induces Type I IFNs, which may play a role in tissue injury and regeneration. 20, 21 We have previously demonstrated that MyD88, a common adaptor to TLR9, TLR2 and TLR4 is critical in sensitization to liver injury.16 Here we employed a model of TLR9-associated liver injury owed to sensitization by the synergistic effect of the TLR9 ligand CpG and the TLR2 ligand LTA, followed by a second hit with LPS,15, 16 and asked if the integrity of the Type I IFN pathway was involved in liver damage. We found that combined administration of TLR9 and TLR2 ligands induced and sensitized the liver to injury by the TLR4 ligand LPS, as indicated by increased serum ALT levels in WT mice (Fig. 1A). More importantly, TLR9+TLR2 ligands induced expression of IFNα (Fig. 1B) and IFNβ (Fig. 1C) mRNA in the liver and expression of both IFNα and IFNβ was further upregulated upon TLR4 stimulation in WT mice. We also found that expression of the Type I IFN-inducible gene, interferon regulated gene ISG15, was induced by TLR9+TLR2 ligand treatment and the expression was further increased upon subsequent LPS stimulation (Fig. 1D). Collectively, these data suggested that Type I IFNs and IFN-triggered signaling pathways were upregulated in TLR9-associated liver injury.
Our data indicated activation of Type I IFN signaling in TLR9-associated liver injury. While both TLR9 and TLR2 ligands activate production of proinflammatory cytokines, TLR9 stimulation also triggers Type I IFNs.17 Type I IFN production induced by TLR9 is largely dependent on activation of intracellular pathways involving interferon regulatory factor-7 (IRF7).22 To define the importance of Type I IFN in TLR9-associated liver injury, we tested IRF7-deficient mice.
In sharp contrast to their wild-type littermates, IRF7-deficient mice showed exacerbation of TLR9-associated liver injury, as indicated by serum ALT elevations (Fig. 2A). Histopathology analysis (Fig. 2B) of IRF7-deficient livers revealed an about 5-fold increase in the number of inflammatory infiltrates (10.33 ± 3.71 in IRF7-KO vs. 1.75 ± 0.48 in WT, P = 0.026) and an about 2.5-fold increase in total area of inflammatory infiltrates (0.67 ± 0.05 vs. 0.28 ± 0.05 mm2, P = 0.017), compared to wild-type controls.
The increased TLR9-associated liver injury in IRF7-deficient mice was accompanied by deficient induction of IFNα (Fig. 2C) and IFNβ (Fig. 2D), compared to controls. LPS stimulation could partially overcome the deficit in IFNα and IFNβ expression in TLR9+TLR2 primed mice, presumably by the direct effect of TLR4 signaling on Type I IFN induction.23 However, there was decreased induction of the IFN-inducible genes, ISG15 (Fig. 2E) and IP-10 (Fig. 2F), in IRF7-deficient mice and further expression of these molecules upon stimulation with LPS was limited. These data supported our hypothesis that Type I IFN induction plays a role in the pathogenesis of TLR9-induced liver damage and suggested a protective role for Type I IFNs in liver injury.
The effects of Type I IFNs are mediated by a cognate receptor composed of two chains, IFNAR1 and IFNAR2, both of which are essential to initiate production of the interferon-stimulated genes (ISGs).24 To differentiate between the direct and indirect protective effects of Type-I IFNs in TLR9-associated liver injury, we tested mice deficient in type I interferon receptor expression (IFNAR1-deficient mice).
Similar to findings in IRF7-deficient mice, mice deficient in IFNAR1 expression showed significantly increased serum ALT (Fig. 3A), widespread liver inflammation, about 5-fold increase in the number of inflammatory foci (4.80 ± 0.49 in IFNAR1-KO vs. 1.0 ± 0.58 in WT, P = 0.018) and about 7-fold increase in total area of inflammatory infiltrate (0.40 ± 0.11 vs. 0.06 ± 0.04 mm2, P = 0.036) after TLR9+TLR2 stimulation compared to wild-type controls (Fig. 3B).
Type I IFNs per se are IFN-sensitive and are strictly regulated by a self-initiated amplification loop involving IRF7 and both IFN receptor chains.24 Consistent with this mechanism, IFNAR1-deficient mice showed substantially lower induction of liver IFNα (Fig. 3C), IFNβ (Fig. 3D) and minimal expression of ISG15 (Fig. 3E) and IP-10 (Fig. 3F), compared to controls. This difference was not overcome by LPS stimulation. Collectively, these data suggested that both Type I IFN induction and IFN-induced signaling may play a protective role in the liver by limiting inflammatory infiltrate and liver injury.
The exaggerated liver inflammatory infiltrate in IRF7- and IFNAR1-deficient mice suggested a role for Type I IFNs in recruitment of inflammatory cells in TLR9-associated liver injury. We thus aimed to define the cell composition of these inflammatory infiltrates. Flow cytometric analysis of liver mononuclear cells (LMNCs) showed equal enrichment of CD68+ monocytes/macrophages in the livers of both WT and IFNAR1-deficient mice after TLR9+TLR2 priming (Fig. 4A). Similarly, liver expression of chemokines MCP-1, MCP-2, MIP-1α and MIP-1β (Suppl. Fig. 1A-E) and chemokine receptors CCR1, CCR2 and CCR5 (Suppl. Fig. 1F-H), which are involved in macrophage recruitment, was upregulated in TLR9-associated liver injury to a comparable extent in both WT and IFNAR1-deficient mice.
In contrast to WT mice, LMNCs isolated from mice deficient in IFNAR1 showed a significantly lower proportion of CD11c+ (myeloid) and PDCA1+ (plasmacytoid) dendritic cells (DC) (Fig. 4B). This finding was associated with a significantly decreased liver expression of the chemokine ligand 21 (CCL-21) (Fig. 4C), a key molecule involved in recruitment of DC, 25 and decreased expression of the CCL-21 receptor CCR7 (Fig. 4D). These data support our hypothesis that in TLR9-associated liver injury, Type I IFNs are required for dendritic cell recruitment to the liver.
The protective effect of Type I IFN induction and signaling against TLR9-associated liver injury implied the involvement of Type I IFN-dependent anti-inflammatory factors. We thus analyzed the expression of another IFN-dependent gene, IL-1 receptor antagonist (IL-1ra), which is a natural endogenous antagonist of the proinflammatory interleukin-1β (IL-1β) at the receptor level.26 Pro-IL-1β gene in the liver (Fig. 5A) and IL-1β protein (Fig. 5B) in the serum were significantly induced by TLR9+TLR2 ligands and further upregulated by LPS to a comparable extent in WT, IRF7- and IFNAR-deficient mice (Fig. 5A,B). Induction of IL-1ra mRNA in the liver and of the secreted IL-1ra protein in serum were decreased both in IRF7- and IFNAR1-deficient mice treated with CpG+LTA, compared to controls (Fig. 5C,D). More important, sensitization via TLR9+TLR2 ligands resulted in less IL-1ra protein production upon stimulation with LPS in both IRF7- and IFNAR1-deficient mice compared to their wild-type controls (Fig. 5D). This finding suggested that aggravated TLR9-associated liver injury in Type I IFN deficient animals is associated with a significant imbalance in IL-1β/IL-1ra signaling.
Our data suggested a protective effect of IL-1ra in TLR9-associated liver injury. To gain a mechanistic insight, we first investigated the source of IL-1ra in the liver. We observed that WT primary hepatocytes and LMNCs stimulated with IFN-α in vitro produced significantly more IL-1ra, compared to non-stimulated cells (Fig. 6A). Next, we asked whether deficiency of Type I IFNs results in differential production of inflammatory cytokines by LMNCs. In vivo priming of mice with TLR9+TLR2 ligands sensitized LMNCs to ex vivo stimulation with LPS and resulted in significantly greater induction of inflammatory cytokines TNF-α (Fig. 6B) and IL-1β (Fig. 6C), compared with LPS-stimulated LMNCs of non-sensitized mice. In contrast to WT mice, LMNCs isolated from IRF7- and IFNAR-deficient mice showed significantly increased induction of TNF-α upon ex vivo stimulation with LPS (Fig. 6B); induction of IL-1β did not significantly differ between genotypes (Fig. 6C).
Consequently, we asked whether IL-1ra could play a protective role in hepatocyte death induced by synergistic activities of TNF-α and IL-1β. Treatment of primary WT hepatocytes with TNF-α did not induce hepatocyte death (Fig. 6D), consistent with previous reports that healthy WT hepatocytes are resistant to stimulation with TNF-α alone.27 However, pretreatment with IL-1β sensitized hepatocytes to TNF-α induced death (Fig. 6D). More important, the sensitizing effect of IL-1β was significantly reduced by IL-1ra (Fig. 6D). Stimulation with IL-1β + TNF-α lead to a significantly greater extent of hepatocyte death in IRF7- and IFNAR1-deficient hepatocytes, compared to WT; significant protection from hepatocyte death was observed after co-treatment with IL-1ra in all genotypes (Fig. 6E).
Taken together, these data suggested that Type I IFNs induce IL-1ra production both in hepatocytes and LMNCs, and that IL-1ra protects hepatocytes from IL-1β-dependent sensitization to TNF-α-induced cell death.
To evaluate the protective role of Type I IFN in TLR9-associated liver injury, we first administered pegylated IFNα2a (pegIFNα2) to WT mice and observed a significant induction of serum IL-1ra (Suppl. Fig. 2). Next, we showed that pegIFNα2 administered to TLR9+TLR2-primed mice two hours prior to LPS significantly prolonged survival (Fig. 7A) and ameliorated TLR9-associated liver injury (Fig. 7B), compared to control mice. Furthermore, pegIFNα2 prevented aggravation of LPS-induced liver injury after TLR9+TLR2-priming (Fig. 7B). Importantly, serum IL-1ra positively correlated with the length of survival (Suppl. Fig. 3A), and negatively correlated with the extent of liver injury (Suppl. Fig. 3B). Accordingly, histopathology analysis revealed reduction in liver inflammatory infiltrate and the extent of necrosis in mice pretreated with pegIFNα2 compared to controls (Fig. 7C). Taken together, these data suggest that type I IFNs induce IL-1ra which has hepatoprotective and anti-inflammatory effects in TLR9-induced liver injury.
To demonstrate the direct protective effect of IL-1ra, we initiated treatment with recombinant IL-1ra in WT mice 24 hours prior to administration of TLR9+TLR2 ligands and continued with IL-1ra throughout the experiment. Mice pretreated with IL-1ra showed significantly prolonged survival after injection of LPS (Fig. 7D), which was associated with lower ALT levels (Fig. 7E) and reduction in liver inflammatory infiltrate and extent of necrosis compared to controls (Fig. 7F). Collectively, these data suggested that Type I IFNs are needed to elicit a strong anti-inflammatory response by induction of IL-1ra, and that Type I IFN-regulated IL-1β/IL-1ra system is key to the protective role of Type I IFNs in liver injury.
TLR9-dependent liver damage is involved in the pathogenesis of several liver diseases, such as alcoholic liver disease,5 primary biliary cirrhosis,6 primary sclerosing cholangitis7 and acetaminophen-induced liver injury,8 as well as in pathological processes such as liver fibrosis,10 liver cirrhosis,11 ischemia-reperfusion injury,12 and liver graft rejection.13 Thus, TLR9 holds the common link between different processes which lead to liver diseases; therefore, unraveling the pathogenesis of TLR9-induced liver injury may aid in identification of novel, efficient pathogenesis-based management or cure. Here we report the novel finding that Type I IFNs have an important regulatory role in TLR9-induced liver injury by limiting inflammation and liver injury. Further, we demonstrate that Type I IFN-induced IL-1ra could serve as a potential therapeutic target in liver injury.
In the current liver injury model, three TLR agonists are being used. Our recent and previous 15, 16 data show that liver inflammation and injury induced in this model are primarily dependent on TLR9; liver damage elicited by CpG is aggravated by co-stimulation with TLR2 and a secondary stimulation with TLR4. Of these TLRs, TLR2, 4 and 9 activate the MyD88-dependent pathway, while IRF3 activation is exclusive to TLR4. Type I IFN and IRF7 induction can occur via both TLR9 and TLR4. 18
We first demonstrated that Type I IFNs, IFNα and IFNs, were induced at the mRNA level in the TLR9-associated liver injury. This Type I IFN was biologically active as suggested by the increased expression of the IFN-inducible genes, ISG15 and IP-10 in the liver. Our novel observation of the increased liver inflammatory infiltrate and exacerbated liver injury in IRF7 and IFNAR1-deficient mice suggested a protective role for the Type I IFN induction in the liver. Indeed, previous studies suggested that Type-I IFNs can mediate anti-inflammatory effects (summarized in 28).
Compared to IFNAR1-deficient mice, where the protective Type I IFN signaling was fully inhibited, IRF7-deficient mice could still produce TLR4-induced Type I IFNs (preferentially IFNβ) via the TLR4-IRF3 pathway. In our study, TLR9-associated liver injury was associated with induction of IFNα, IFNβ and interferon-stimulated genes in wild-type mice. Notably, IFNAR1-deficiency abrogated the induction of Type I IFN response to much greater extent than IRF7 deficiency. Also, IFNAR1-deficient mice showed the most severe TLR9-associated histological liver damage, which exceeded the extent present in IRF7-deficient mice. The different observation between IRF7- and IFNAR1-deficient mice could be explained by differential composition of inflammatory liver infiltrate, or by the fact that Type I IFNs are potentially inducible by multiple pathways, including IRF1, IRF3 and IRF7.23, 29 Therefore, protective Type I IFNs could still be induced in IRF7-deficient mice by TLR9 in an IRF7- independent, IRF3-dependent manner, while the downstream protective effect of Type I IFNs is completely abolished in IFNAR1-deficient mice which cannot respond to type I IFNs.
We found that deficient Type I IFN signaling was associated with decreased liver recruitment of dendritic cells and with decreased expression of CCL-21and CCR7, a key chemokine-receptor pair involved in dendritic cell trafficking.30 Our novel findings indicating a role of Type I IFNs in recruitment of dendritic cells and in expression of CCL-21, together with data showing that TLR9-activated dendritic cells are key producers of Type I IFNs,31 suggest a novel self-sustaining mechanism for dendritic cell recruitment into the liver. It has been reported that dendritic cells are essential for Th1 response in the liver induced by TLR9 + TLR2 ligands 32 and contribute to liver fibrosis,9 Consistent with earlier observations15 TLR9-induced inflammatory infiltrates, that require dendritic cell recruitment to the liver,32 amplified pro-inflammatory cytokine induction by LPS. Our novel data suggest a dual role for dendritic cells in the liver. First, dendritic cells are necessary for TLR9-induced inflammatory cell infiltrates and sensitization to TLR4 ligands. Second, dendritic cells provide anti-inflammatory signals mediated by Type I IFNs.
We observed a synergistic effect of TLR9 + TLR2 and TLR4 ligands in upregulation of IL-1ra in wild-type animals; both IRF7-deficient and IFNAR1-deficient mice showed decreased induction of IL-1ra, compared to WT. One can speculate that this synergistic effect of TLR ligands on IL-1ra induction is mediated by Type I IFNs and IRF7. This notion is consistent with our data showing a synergistic effect of TLR9+2 and TLR4 ligands on Type I IFN expression in wild-type mice. We observed that Type I IFN induces IL-1ra in hepatocytes and liver mononuclear cells, and that IL-1ra protects hepatocytes against the sensitizing effect of IL-1β towards cytotoxicity induced by TNF-α. Our findings support previous reports that in order to become susceptible to the cytotoxic effect of TNF-α, hepatocytes require priming with ligands that interfere with their proliferation.27 Indeed, IL-1β has been shown to inhibit DNA synthesis in rat hepatocytes.33
We further showed that administration of recombinant pegIFNα2 induced IL-1ra in vivo. This finding was in agreement with our in vitro data from hepatocytes and liver mononuclear cells, with in vitro data that IL-1RA promoter region contains Type I IFN-inducible elements,34 and with data demonstrating increased in vivo production of IL-1ra upon treatment with recombinant IFN in humans.35 In addition, we observed that in vivo administration of pegIFNα2 significantly ameliorated TLR9-associated survival, liver injury and inflammation.
Our novel data demonstrated that pretreatment with recombinant IL-1ra significantly ameliorated liver injury and inflammation in WT mice. These findings confirm the anti-inflammatory effect of IL-1ra in liver injury and are complementary to study of Iizasa et al.36 who showed that deficiency of IL-1ra resulted in exacerbated liver injury and inflammation induced by Propionibacterium Acnes, which activates TLR9 and TLR2 receptors.15, 16 Our results show for the first time that Type I IFNs potentially protect from liver injury by inducing anti-inflammatory IL-1ra.
IL-1ra acts as a natural antagonist of IL-1β,26 and we show that in the liver IL-1ra is produced by both hepatocytes and liver mononuclear cells. Our data also demonstrates the protective effect of IL-1ra in TLR9-associated liver injury and survival. In previous studies, Imaeda et al.8 showed that in acetaminophen hepatotoxicity, inflammatory response is triggered by apoptotic mammalian DNA that increases transcription of IL-1β, and that inflammatory response is ameliorated in mice deficient for TLR9 and in mice treated with anti-IL-1β antibody. Importantly, IL-1ra has been reported for the treatment of hepatic failure in rats using a bioartificial liver device.37 These studies support our finding that the balance between IL-1β/IL-1ra is of crucial importance in TLR9-induced liver damage (Suppl. Fig. 4).
In conclusion, our findings suggest that the endogenous anti-inflammatory signaling induced by Type I IFNs and mediated by IL-1ra regulates the extent of TLR9-induced liver damage, and support the indispensable role of Type I interferon signaling in immune mediated liver injury. Finally, we suggest the potential role of IL-1ra in therapy of TLR9-associated liver diseases.
Financial support: This work was supported by PHS grant # RO1DK075653 from NIDDK (to G.S.). Core resources supported by the Diabetes Endocrinology Research Center grant DK32520 were also used.
Jan Petrasek - Acquisition of data, analysis and interpretation of data, statistical analysis and manuscript writingAngela Dolganiuc - Acquisition of data, analysis and interpretation of data, and manuscript writing
Evelyn A. Kurt-Jones - Intellectual content, critical revision of the manuscript
Timea Csak - Acquisition of data, analysis and interpretation of data
Gyongyi Szabo - Study concept and design, critical revision of the manuscript, and obtained funding.
Disclosures: nothing to disclose
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

domain: biology


Citi Research released a new report yesterday titled “Energy Darwinism – Key Equity and Commodity Debates”. The report continued to develop Citi’s theme of “Energy Darwinism” to describe the ongoing structural evolution of the utilities and energy markets in the 21st century. Citi Research analysts Jason Channell and colleagues who authored the report point out that first world countries now spend more on renewable capital expenditures than they do on conventional generation, and that interest in solar power and other renewable forms of energy continues to grow rapidly worldwide.
Energy market: Japan rapidly installing solar power
The report highlights how Japan is catapulting itself into a top solar power producer in an amazingly short period of time as a response to the 2011 Fukushima nuclear disaster. “Japan has introduced the world’s most attractive subsidy scheme for solar and is installing capacity equivalent to 9 nuclear power plants in the space of one year. Japan could have the same level of solar installed as Germany in half the time.”
Energy market: Electricity storage
Fusion power and cheap, high-capacity electricity storage are the two holy grails of the energy industry. Fusion power is probably still at least a decade away, but the cost-effective, high-capacity electricity could be available in just a few years. Channell et al. elaborate on the transformative nature of such a technology, but suggest potential commercial applications are still several years away.
Stone House Capital Partners returned 4.1% for September, bringing its year-to-date return to 72% net. The S&P 500 is up 14.3% for the first nine months of the year. Q3 2021 hedge fund letters, conferences and more Stone House follows a value-based, long-long term and concentrated investment approach focusing on companies rather than the market Read More
Energy market: Distributed generation
The report also mentions distributed generation as another potential wildcard in the ongoing reshaping of the energy sector. Distributed generation is energy generated at points of use, such as rooftop solar installations on individual homes.
Channel and colleagues detail the argument. “One implication of this is that this power itself does not necessarily go through the grid (though it may, the other way, if exported back), resulting in lower grid usage. However, the grid must still be maintained, and hence lower utilization is likely to push per unit charges higher, with yet another upward pressure on bills.”
Energy market: Cheap natural gas from rapid development of U.S. shale fields
The development of the technology to extract natural gas from shale formations marked a sea change in domestic natural gas prices and has sparked a significant revamping of the power generation and utilities sectors to take advantage of cheap gas. Citi’s analysts also point out that this trend is really just getting into full swing, and that companies in this sector must keep their thumb on the pulse of technological and market developments.


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Timelines Gold Award Laudation
The site "Toledo- Bend Gallery" has a beautiful layout and is easy to navigate, there is an additional navigation at the bottom of every page. All parts of the site are divided into several submenus, where Frank Dutton shows beautiful images from the area of the Toledo-Bend Lake. Small preview images open in a bigger shadowbox.
On his images the author shows the various activities on and around the Toledo Bend Lake. In his wildflowers gallery you can see wonderful macro photos.
The webseite Toledo Bend Gallery has a valid HTML code and CSS.
Congratulations, the website Toledo Bend Gallery wins Timelines Gold Award of Excellence, Timelines' Top Award

domain: geography


In a thunderous announcement that has set the entire fandom on fire, the highly anticipated sequel to the blockbuster film RRR has just been officially confirmed! Brace yourselves for another epic chapter that will send shockwaves through the cinematic universe. The news has spread like wildfire, igniting an electrifying buzz among fans who are eagerly awaiting the next thrilling instalment.
Although the details are being kept tightly under wraps, the word on the street is that the film's production will kick off in no time, setting the stage for a mind-blowing adventure. As for the cast, the suspense is killing us all. Who will step into the spotlight this time? The suspense is tantalizing, leaving fans on the edge of their seats, eagerly speculating about the line-up of stars that will grace the silver screen.
Taking to the realm of social media, the esteemed Manobala Vijayabalan dropped a bombshell tweet that sent shockwaves across the digital landscape. “#RRRMovie sequel CONFIRMED. “We are planning to make a sequel of #RamCharan - #NTR’s #RRR. It will be in Hollywood Standards. The movie will either be directed by SS Rajamouli or someone under SSR supervision. Mahabaratham : The dream project of SS Rajamouli will commence very soon after the completion of Mahesh Babu’s jungle adventure film.- Vijayendra Prasad."
The ecstatic response from fans flooded the comment section, leaving no doubt that this news has unleashed a hurricane of excitement
Let's rewind for a moment and relish the phenomenal success of its predecessor, RRR, an action-packed marvel that captivated audiences worldwide. This magnum opus not only conquered hearts but also achieved the unthinkable, securing a coveted spot in Oscar's history. Yes, you heard it right! RRR stands tall as the first-ever Indian feature film to receive an Oscar nomination, an extraordinary feat that sent shockwaves through the film industry.
Adding to the glory, the mesmerizing song 'Naatu Naatu' by the maestro himself, MM Keeravani, clinched the highly prestigious Best Original Song Award at the 95th Academy Awards. Talk about making an impact! RRR transcended boundaries and left an indelible mark on global cinema.
With SS Rajamouli at the helm, this blockbuster extravaganza boasted an ensemble cast of superstars, including the charismatic Jr NTR, the dashing Ram Charan, the enchanting Alia Bhatt, and the legendary Ajay Devgan, to name just a few. Their collective brilliance illuminated the screen, turning RRR into a mesmerizing spectacle that left audiences craving more.
Now, as we eagerly await the sequel, our imaginations run wild with possibilities. Buckle up, movie buffs! The journey is about to begin anew, promising adrenaline-pumping action, unforgettable performances, and a captivating narrative that will push the boundaries of cinema itself. RRR's legacy continues to shine bright, and its sequel is poised to redefine the very essence of blockbuster entertainment. Get ready for a rollercoaster ride that will leave you breathless, exhilarated, and craving for more. The countdown has begun!


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I just finished two books that incorporate innovative forms of content beyond the printed word (and no, I'm not talking about digital ink, either). I'll get to those titles in a sec, but first I wanted to take a litle trip down Memory Lane, to the good ole days of 2007 and a little known book called The Invention of Hugo Cabret. Of course I'm being facetious. If you're one of about a dozen people who haven't heard or read this book, do it. But the point I want to make about Brian Selznik's "massive," 533-page middle grade novel is this: it won the Caldecott. You might recall that the Caldecott is awarded for illustration of a children's book.
Wait a minute. A novel winning an award for illustration? Well, yeah. And at 25K words, it's an easy guess (if you haven't read or seen the book yet) what fills those 500+ pages.
Selznik's book wasn't the first to mix word and image, but I think with the Caldecott win, it really ushered in the idea that the novel as we know is evolving to become more mixed media. (This ignores, for the moment, that graphic novels, or GNs, have been becoming more and more popular and complex of late. But GNs are separate thing altogether. I'm talking more about how the traditional novel is changing.)
Without a doubt, we are well along in a revolution where the written, printed word is becoming heavily encroached upon by images, video and audio content. And while traditional novels (both paper and ebook) will be around for a long time to come, they will have to compete more and more with stories that incorporate mixed media.
For example, I just finished Malice, Chris Wooding's paranormal 68K-word mixed novel/graphic novel. The interesting thing about this book is that, while the story could easily stand on its own, the graphic novel really adds a new dimension that children today will connect with, especially boys. And if that gets them to read, great. Remember, to publishers more readers means more sales.
The other book is Patrick Carman's Trackers, released last week, about a group of four teen tech geeks. The story follows an interview of the MC as he recounts the events leading to the present (I'm being purposefully coy here to avoid giving anything away). The book could be read from cover to cover without leaving its pages, but the reader is cued to logon to a website, enter codes, view videos and crack codes, thus becoming a participant in the story.
It's an interesting concept and a challenge for the traditional writer to consider. Will it be successful? In my opinion, as long as the reader has to physically leave the comfort of their chair/bed/hammock or whatever, no. But we are fast approaching an age where all these sources of content will soon be available all at once and from a single device. I think stories where the reader (soon to become "audience participant") can seemlessly shift between the active experience of reading and the passive experience of watching/listening, while also enjoying a little bit of both in interactive ways too, will become more popular.
Why is this happening?
I don't think this has anything to do with shorter attention spans or being bombarded with information from a hundred different sources all at once, or sensory overload. I think it's only natural to want to experience things more fully. And if a story can be experienced more fully (which is not to say totally passively, as films do), then it will succeed.
What does this mean to the author of next generation stories?
Well, first and foremost, I don't think it has to mean anything to any one author. As I said before, traditional books will be around for a long, long time. But they will compete with mixed media going forward. I think authors of children's lit content should keep all this in mind. Writers should think about whether and how they should access these new media to assist them in telling their stories, whether through image, video, audio or whatever comes next (olfactory?). Do you see an opportunity to turn your novel into a mixed novel/GN or tie-in the internet for expanded experiences?


With SmartWire-DT, Eaton has heralded in a new era of connectivity between individual switchgear and controllers. SmartWire-DT not only replaces the control circuit wiring for all the components inside a machine's control panel, but also extends this flexibility to elements such as sensors. This way, SmartWire-DT makes it perfectly possible for a system's central controller and moving components to communicate with each other continuously and directly. In addition, the fact that this eliminates the need for previously required PLC inputs/outputs and control wiring saves signifi-cant space, making the use of more compact control panels possible.
The SmartWire-DT communication system can be used anywhere where switchgear, sensors, and actuators are at work. And the advantages it holds over competing solutions quickly become clear during installation, operation, and further expansion down the line. Large data volumes, a length of up to 600 m, and flexible options for connecting to field buses from virtually any PLC manufacturer are just a few of the characteristics that make SmartWire-DT the ideal system for an extremely wide range of applications.


Maddman: The Steve Madden Story (2017)
Maddman: The Steve Madden Story Movie Details :
Maddman: The Steve Madden Story Summary
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Witness the incredible rise, fall, and resurrection of Steve Madden, the entrepreneur who launched a billion-dollar fashion empire with $1,100, and whose branded shoes are now in the wardrobes of millions of women and men around the world. The film provides intimate access to Madden as it explores how he repeatedly nearly destroyed his life through drugs, through alcohol, and through a single-minded determination to build his business no matter what the cost to his personal life, and even to his freedom. Here is the man behind the myth depicted in the Martin Scorsese film “The Wolf of Wall Street”. Throughout it all, Madden has maintained an uncanny charm, clever wit, endless creativity, and a keen instinct that has shaken the fashion world to its core. Is Maddman: The Steve Madden Story on Netflix? Watch Maddman: The Steve Madden Story streaming online via the link(s) above.


No it's not, it's a crippled Phenom I aka Agena. AMD never made any K10 dual core processors at 65nm.
OP, I doubt yours will unlock, the majority of them never did and reports of them unlocking didn't come out until near the end of their manufacturing. Enable ACC and you'll see if it does or not, but I know mine never did anything with ACC.
Actually Uncfan, Loneninja was correct. The 7750 is a Kuma dual core which was nothing more than an Agena phenom with 2 disabled cores. There are 2 more cores on that die. At the time, AMD was still producing the last of the Brisbane X2 chips. Those were the native dualies. Native Phenom based dual core chips didn't come around until after the 45nm die shrink.
As for unlocking, I have not heard of it being done on the Agena chips at all. That may be due to the fact that AMD had lower yields and a larger percentage of the disable cores were actually defective. It could be it just didn't work on the Agenas, or perhaps fewer people had ACC available since the SB 750 was released fairly late in the Agena cores lifecycle and the 710 even later.
Give it a whirl. See what happens and let us know.
there have been very little if any attempts to unlock these cpus because unlocking a dual core 7750 with its 95 watt tdp would result in a chip with a 190watt tdp
btw only intel has been known to glue dies together, all amd duals quads and hexas have been native, exept for the recently released opteron 12 core which is connected by 4 dedicated hyper transport links, not thru fsb like intel


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Walter's Opening to Deep Glen Bay
The is the quintessential coastal traverse: challenging, committing and varied (with at least four major rock types), with an unusually strong sense of adventure and the unknown.
Due to the length of the traverse, the difficulty of escape and the exposed nature of the coast, this traverse really deserves respect and care. It may be possible to escape in one or two places, but even when there is no cliff, the land is extremely steep and the bush is sometimes very dense.
Drive to the car park for the walk to Cape Surville. The walk from here to Cape Surville is highly recommended in its own right, and a good way to get an impression of the first half of the traverse. It is immediately clear that the coast is extremely cliffy, and access to the water's edge is difficult. From the car park, head north down to the creek bed of Chasm Creek, then follow this (an interesting sunken corridor) down to the "chasm": a deep cleft in the cliffline into which the faint creek tumbles: this area is marked as Walter's Opening on some maps.
The chasm must be descended. The waterfall falls into a dark cave with a pond, a touch over waste depth and with a bottom of small to medium sized boulders and rocks. It is easy to clamber down most of the way, but unfortunately, the final five metres of the chasm is both slippery and at least vertical, and probably too high to safely jump from because of the shallow water depth. We slid down an old tree trunk that was stuck in the chasm. It might be worthwhile bringing a rope here, in case a tree trunk is not available.
Our first attempt was aborted just after this this point. The swell was too big and we had a serious scare when cornered by a large wave while inside a nearby cave (method of survival: "hang on very tight" seemed to work on this occasion).
The second attempt was made on a day in November with a forecast of 15 degrees, showers and possible highland snow. We started at dawn, with mostly clear skies and low swells.
Initially the rock is a kind of mudstone perhaps: certainly it is quite loose, though at water level it is polished and even provides occassional short overhanging sections. The climbing is mostly short and scattered in this section, but the coastline is interesting, with some large caverns and hidden coves: a particularly striking arch is encountered shortly before the bay starting Cape Surville (see pictures). There are some short swims required.
By the time the start of Cape Surville is reached, the rock has turned to dolerite, and there are some lengthy sections of moderately easy climbing (with some very short swims) on typical good quality coastal Tasmanian dolerite. The point of Cape Serville itself is quite impressive, with some daunting dolerite caves capped by a some kind of very crumbly sedimentary rock/soil. The cliffs are probably over a hundred metres at their highest. Some moderate swims are required to pass the caves.
At Deep Glen Bluff the rock makes a dramatically sudden change to granite: the southern most section of granite on mainland Tasmania. The bluff itself continues for a long way, and presents some of the longest unbroken pieces of coastal traversing I've done. In many places, the soils above the cliff seem to have leached a layer of what looks to be classic smooth limestone over the granite. At one point this completely takes over, with no sign of the granite beneath. One section of rock offers consistent climbing on pristine granite/limestone at around grade 15 to 17 for hundreds of metres without break.
When the bay of Deep Glen Bay is reached, the granite takes on a different kind of character, presenting a series of sharp ribs of rock that force many short swims. Around 7 were needed within the bay itself. This was particularly memorable on the successful traverse, as rounding the corner to the bay (which is, ahem, deep) presented us with a biting southerly wind with blasting showers. The base of Deep Glen Bay itself has amazing character and presence (as well some historical interest) and is a fitting place to finish this brilliant traverse.
The adventure is not yet over however: the car is now some distance away. There is a faint track up the gully leading to Deep Glen Bay: this is very steep, but filled with beautiful forest of giant ferns, and some enormous Eucalyptus Globulus toward the top. At the top, a fire trail is reached. Head rightwards and then down another track that heads roughly northward back toward Cape Surville. Follow the Cape Surville track back to the car. The walk to Deep Glen Bay is described in several walking books, and it would be worthwhile investigating these first.
This round trip took a full morning: around 7AM to 1:30PM; we went fairly fast, doing a fast jog for the walk back.
The section north of Cape Surville: we emerged from within the cave in the middle left of the picture (the "arch" described in the traverse description).
Beautiful easy bay between the cave and Cape Surville.
Click on photos for larger image.
From the top of Cape Surville looking north. The start at chasm creek is out of view to the right of picture.
The northern side of Cape Surville offers a reasonably extended section of dolerite climbing above water. The rock is also dolerite on the southern side, but the coast is pockmarked with several very dramatically imposing caves.
The Sisters, off the northern corner of Deep Glen Bluff. There is a very dramatic change from dolerite to granite here (at the enormous diagonal stripe; with a kind of crumbly mudstone/limestone on the hill above). The longest sections of climbing are south of this point.
All photos by Peter Jackson.


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“For every woman who commits suicide after their divorce, nine men commit suicide after their divorce (Kposowa A. J. 2000).”
We’re going to get into the reasons for this statistic, but before we do that, know that if you’re living that hell right now and you’re looking for help, I’m a clinician in Orlando, Florida, and I will talk with you if you’re on the edge. Call me at (407) 777-2524 or come see me in my office.
If you are in crisis, call the toll-free National Suicide Prevention Lifeline at 1-800-273-TALK (8255), available 24 hours a day, 7 days a week. The service is available to anyone and all calls are confidential.
What People Say about Men who Commit Suicide After Divorce
When I ask why men commit suicide after divorce, the #1 reason I’m given is that they don’t want to pay child support or alimony, but this doesn’t make sense. A man who spent his time pre-divorce providing for his family will now kill himself because he still has to provide for his kids? I don’t think so.
Some people say men commit suicide because they can’t handle the rejection of their soon-to-be ex-wives. While this may be the case, it’s not even a significant portion of the minority of situations. The ending of a relationship–good or bad–can be difficult, but is seldom a motivator for ending your own life.
Far too often we see that men commit suicide because they have been separated from their children. I get that there is this rampant misconception that all men are deadbeat dads and that women are better caretakers. This is a cultural fantasy that has a real and devastating effect on the man–an effect that is causing men to commit suicide because their children are being stripped away from them by the courts and/or the wives they are separating from.
Please, keep on perpetuating this idea if you’re fine with contributing to more men committing suicide.
2 Reasons Men Commit Suicide after Divorce
First the court system takes the man apart, dehumanizing and demonizing him as a deadbeat dad. Then, he pays up to 50% of his income on alimony/child support and another 30% in taxes without a sliding scale (in case his business fails). Finally, after all of this, he comes into his feelings–if he’s even made it to this point. He feels as if he has no future and as if his children no longer see him as “Dad”, but rather as “him”.
After the divorce, the man no longer sees what is future can be because he has just lost the future he had previously been creating. Now his wife, children, friends, and social communities have been split up like all of his other assets, many of which are now unavailable to him entirely. He is struggling to pay everything mandated by the courts so he can stay out of jail and he’s doing all of this without the social support he could previously rely on.
Is it becoming more clear why hopelessness sets in and the man starts to consider or commit suicide? He has been humiliated and he has lost his children, income, home, stability, future, and emotional bonds.
The same people who claimed that men commit suicide because they don’t want to pay child support will now say that divorce is almost always the fault of the man because he cheated on his wife. They have a skewed understanding of the relationships between men and women and are operating under the pathological defense where women and men are split along the lines of good and bad, respectively. These beliefs are irrelevant to fact and anyone who holds them needs to learn more about the subject.
If you feel like you’ve been completely fucked over by your divorce and things are happening in your life that you’re struggling to handle, Make a Contact and/or call the toll-free National Suicide Prevention Lifeline at 1-800-273-TALK (8255).
There is a future after divorce and there are men out there who will sit with you in your hell so you can get there together.
- Kposowa A.J. Marital status and suicide in the National Longitudinal Mortality Study. Journal of Epidemiology and Community Health 2000; 54: 254-261.

domain: psychology


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It would have been an entirely different movie without her
Imagine a world where Meryl Streep didn’t play the iconic Miranda Priestley in ‘The Devil Wears Prada’.
Back before the 2006 hit film came into our lives, this was almost a reality.
The movie’s producer, Wendy Finerman, recently revealed that Streep was almost passed over for the role of the New York City-based editor-in-chief of the fictional fashion magazine, Runway.
Finerman shared on the ‘Hollywood Gold‘ podcast that this was down to one person on the production team’s opinion of the actress.
The producer told the podcast’s host, Daniela Taplin Lundberg, that the person in question wanted to rule her out because they felt the ‘Mamma Mia’ star had ‘never been funny a day in her life’.
“And Meryl, people thought we were crazy. I mean, I had people call me up and say, ‘Are you out of your mind? She’s never been funny a day in her life,’” Finerman recounted.
How wrong they were.
“But this was clearly a different kind of world for her,” alluding to many of Streep’s more dramatic film roles.
“I think that that was part of the fun of the unexpected.”
While it was back and forth on the ‘She-Devil’ actress, according to Finerman, Anne Hathway was always their number one choice for the role of Andrea Sachs, Miranda’s junior personal assistant.
This was down to casting seeing Hathaway as ‘a good, all-American girl’.
Wouldn’t like the be the person who doubted Meryl Streep!
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domain: celebrity


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It all started when Dil Raju announced the title 'Ramayya Vastavayya' a few months ago, followed by tweets from Harish Shankar. It was one of the fastest trending topic for a while after that. The sweetness continued when the first teaser was released with NTR singing and dancing around a pole, teasing his girl Samantha, a zone which he would have forgotten long ago. The sensitivity, sensibility was quite evident and positive vibes were around the film building great expectations since then. So, when the team announced the audio launch, expectations went rocket high.
The cloudy cool breeze set the tone for a pleasant event that was to follow. The guests were smiling all the way thru the evening. The auditorium was clapping forever and the friendly atmosphere, filled with genuine enthusiasm was felt complete with NTR's entry clad in a jeans and sky blue shirt tucked in much like a college student than a thigh thumping factionist. The mood continued and would have haunted each and every spectator in the event or everyone who watched it LIVE on TV for a while.
Ace actor Kota Srinivasa Rao said Harish Shankar has a clarity and unlike many directors, he acts and shows. I know him from childhood. I can say this is a Telugu film with a Telugu hero and a tasteful producer. Film will do weel at the Box office too. Editor Goutham Raju said he was thrilled to see the trailer on the big screen though he edited it. Actor Rao Ramesh said Harish Shankar, NTR and Chota ragged him thru the production. It's a great production with a great team and wonderful atmosphere around. I played a great role and it's a thrilling experience all in all.
Writer Satish Vegesna said I just followed director in designing the screenplay for the powerful NTR. Lyricist Sri Mani said I was shaken when I was told I was to write the Intro song for NTR but director Harish motivated me to give the song... Bhaskarabhatla said Reason for the good output is Harish. You will see great one liners even in the songs. Sahiti said NTR has the best music sense and Harish has a command. Anath Sriram said Dil Raju has given me all the important milestones and I thank Harish for this film. Choreographer Bhanu said Thanks to NTR, biggest opportunity to me, Thank you. Chota K Naidu said I am excited about the team and eager for this film to hit the screen.
Guests included prominent writers, producers and directors who have done, are doing or will do projects with NTR.
Koratala Siva said I have seen the songs and so inspired now to design NTR for my next with him. I am eagerly waiting to see the one-liners in the film coz Harish has a great blend of class and mass in him. KL Narayana said 'I know how energetic NTR coz we had a good success in Rakhi with him'. BVS Ravi Kumar said 'One director with a firm grip on the language is Harish. NTR looks so handsome on screen, I feel in love straight away' Gopichand Malineni said 'I was flattered with the first look itself and expecting a lot from Harish and Dil Raju and NTR'. Burugupalli wished the team luck.
'I can See Brindavanam Magic': Vamsi Paidipally
Vamsi Paidipally said 'I feel nostalgic coz I recall the launch of Brindavanam audio three years ago and I feel parallels to the same film. Harish has great positive energies around him'.
'NTR Looks Like a Lover Boy': VV Vinayak
VVV said 'NTR looks quite different in this film... Like a college student, like a lover boy and I wish this film blasts all the records'.
'Looks Like a Celebration, Not a Launch': SS Raja Mouli
Raja Mouli said 'I am floored by the trailer. Dil Raju is a producer who starts with the script, not a combination of hero and director. I congratulate him. Harish Shankar has gone thru ups and lows but hasn't changed at all. His humor didn't change a bit. I loved the montage of your smiling moments. This looks like a celebration, not a launch'.
'Great Team': SS Thaman
Thaman said 'It's important to have a great team. And I am so happy to be a part of this team. RV will be marked by four P's... Harish Possessiveness for the film, Dil Raju's Passion, Chota's Perfection and NTR's Power'.
'Feel The Positive Vibes': Dil Raju
Dil Raju said 'I started my journey as a distributor and so, I invited my RP Road friends too. NTR was carved by VVV, Raja Mouli and Vamsi Paidipally thru their films. Harish has shown him in a new look again. The positive vibes around the film inspire me and I thank the hero and director for the film's output. Harish's journey with all the cast and crew members is worth praise. The film will grow above your expectations and I promise you that'.
NTR Is Young 'Only By Age': Harish Shankar.
Harish said 'I met NTR as a writer few years ago and the relation with him over the years grew and I am indebted to him for treating me as a friend than a professional. They say he is young in age, I say he young 'Only' by age. He is bigger in stature. I doubt if you will see another hero like him in future. He is a hero off screen too. There are very few instances where he had a retake. He is strikingly handsome in the film, I promise. I have a wonderful relation with SS Thaman. He understood the film so well and that will be visible on the screen. I learnt a lot from Chota thru the production. The support I got from everyone made me complete the film with confidence. Gautham Raju, Ram Laxman, art director Brahma and all the other technicians, the girls Samantha, Shruthi Hassan and Hamsa Nandini... My dream has come true with the film... Of doing a 'Dil Raju Film' and an NTR starrer. Dil Raju is a producer the industry needs just because of his command over the production. VVV unveiled the CD pack and gave the first CD to SS Raja Mouli followed by the customary photo op.
'My Directors Helped Me Evolve': NTR
NTR said Actor evolves over the years as he goes thru his films. But its my directors who made me evolve thru their characterizations. VVV , Raja Mouli and Vamsi helped me realize, get motivated to be a young tiger or a warrior. The believed me that I could deliver in Aadi, Simhadri or Brundavanam. Krishna Vamsi made me believe that I can emote, I can be sensitive, I can cry.
Harish helped me go back in timeline, to my college days and believe that I can follow a gal like a collegiate, tease a gal like a teenager does... I asked him many times thru the production if he was satisfied with my performances coz I was coming out of my zone of massy roles to play a college student. He said he was confident and clear coz its his dream of eight years.
Raju-Sirish-Lakshman have been travelling hand in hand with me ever since I met them on the sets of Aadi as distributors... In my highs and lows, my laughs and cries. I wish this continues forever. Thaman has a great rhythm sense and I have been quite inspired by the way he created each music bit imagining me on screen dancing to the tune. Chota the guy that has the greatest command over my face and body language.
He guided me thru the shooting every day discussing and briefing me about the scenes next day. Kota did a small but highly inspiring role. I thank each and every cast and crew member, including the art department, lyricists, especially the direction department who loved the movie as much as I did... NTR concluded saying 'I wish the God and the fans your blessings continue to shower thru my life'.


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New Delhi: The Samyukta Kisan Morcha (SKM) – an umbrella body of over 40 farmers’ unions that spearheaded a protest against the since repealed farm laws – has decided to launch a ‘defeat BJP’ campaign in Gujarat.
Hanan Mollah, one of the most prominent faces of the SKM, said that farmers’ leaders will do small rallies and unite people against the ‘anti-farmer party’ during the campaign in Gujarat.
“We will not participate directly in the election but will appeal to the voters to ask political parties about their stand on debt waiver and the SKM. We will urge the people to ask political parties about MSP too,” said Mollah, adding, “farmers’ leaders will soon hit the ground in the state.”
Leaders will raise issues such as the problems faced by the cotton and groundnut farmers and the issue of lumpy skin disease during the ‘defeat-BJP campaign’.
“On the Constitution Day (November 26), farmers will march towards the Raj Bhawan in Gandhi Nagar and a memorandum will be submitted to the President through the governor, seeking legally guaranteed MSP for all crops,” said Mollah.
As per the SKM, memorandums will be submitted to the President through governors across India, seeking a legal guarantee for the MSP on November 26.
The Modi government constituted a committee on MSP in January this year but the SKM has rejected the committee.
“The committee included five government’s loyalists (representatives of other farmer organisations) who openly advocated all three anti-farmer laws,” it said.
The SKM will also press for a comprehensive crop insurance scheme, complete loan waiver, and pension of Rs 5,000 per month to all marginal, small, and medium-scale farmers during the campaign.
The SKM has also come down heavily on the government for giving clearance for the GM mustard seeds.
“It is a move to facilitate corporate profiteering through seed monopoly, without adequate scientific research on the impact on environment, nature and on the life of humans and livestock,” said the SKM in a statement.
The SKM had campaigned against the BJP during the UP Assembly polls earlier this year. Though it failed to prevent the party from retaining power, they were successful in galvanising the anti-BJP forces on the ground.


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Some wounds need more than time to heal...
I don't remember what it's like not to be scared.
And then I meet him.
My brother's friend and ex-partner is everything I'll never be. Sexy, confident, and perfect. He calls me sunshine and tells me I'm beautiful. He asks me to stay.
When my past comes back with a vengeance, he proves just how much he'd risk to shield me from the demons that were never supposed to resurface.
Readers love Smith and Mellie's story that delivers all the feels!
"This story gets a big ol' WOW! 10++ stars & all kinds of nail-biting!" ~ Carrie M
"Having recently become addicted to Anna Brooks' writing I was anxiously waiting for this one and it was everything I expected it to be...and more." ~Mary A
"In Fixing Fate, Anna introduces us to Mellie and Smith and weaves their love story so beautifully. It's sexy, touching, heartbreaking and sweet, all in one. Safe to say, I'll buy whatever Anna's selling because her books are just that good!" ~ Brenna R
"I honesty went into this book skeptical that it would live up the other reviewers expectations, BUT oh boy was I wrong. This book contains every emotion in the book and will drag you right down with the characters,though it is so worth it when your heart swells from how sweet, caring, and protective Smith is afterwards. Definitely pick this one up and dive in with Smith and Mellie because it was be so worth it." ~Amazon reviewer
Love the suspense
This was my first book by this author and I really enjoyed it! There was a little bit of humor and steam but also the emotions in the story were very real. The heroine had gone through a very traumatic event in her life and while she was able to cope as an adult her past comes back to haunt her. At that point the author gives us an explosion of suspense and from there I couldn't put the book down. I needed to know what was going to happen and how it was going to happen. Overall, I really enjoyed this story and I am looking forward to reading more.
Great story line!
I was absolutely hooked! The plot and just the entirety of this short book was amazing. I loved it!
Couldn’t put it down
Great book, real page turner