If there?s such thing as an ?easy sell? in our house, nothing pleases everyone more than absolutely anything I make whose name starts with chocolate. In fact, my kids? cheers of joy usually drown me out before I can even get the whole word out of my mouth.
Take these Chocolate Muffins for instance. Recently, my two little angels were in the midst of a quarrel at the kitchen table and I was starting to lose my patience from all the bickering. Using my best diversionary skills I announced to them, ?I made chocol??. They were sold before they even knew what it was that I made ? amazing, the power chocolate in any form has over my kids. After each of their first bites, there was peace in the world (at least momentarily)?.and something delicious in their tummies.
These chocolate muffins are light as a feather, but also pack a rich punch of chocolate. The next time you?re trying to grab everyone?s attention, just whip up a batch of these and watch what happens!
*The ever sweet and talented Recipe Girl posted these muffins on her site last week, but just in case you didn?t see them and wanted to make sure you got to see them here!
Chocolate Muffins (Makes 12 regular-sized or 4 mini muffins)
1 1/2 Cups All Purpose Flour 1/2 Cup Unsweetened Cocoa Powder 1/2 Cup Granulated White Sugar 1 1/2 Tsps Baking Powder 1/2 Tsp Salt 3/4 Cup Milk 1/3 Cup Vegetable or Canola Oil 1 Large Egg, beaten
1. Preheat the oven to 400? F. Grease 12 regular or 24 mini muffin tins. 2. In a medium bowl, sift flour, cocoa powder, sugar, baking powder, and salt. 3. In a large bowl, whisk together the milk, oil, and the egg. Add the dry ingredients and stir just until combined. 4. Fill the muffin cups 2/3 full. 5. Bake 18 ? 22 minutes, or until a wooden pick inserted into the center comes out clean.
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This entry was posted on Tuesday, March 6th, 2012 at 6:45 am and is filed under All Recipes, Big Kids Recipes, Desserts, Snack Treats, Toddler Bites, Vegetarian, breakfast. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.
[unable to retrieve full-text content]AP - Military officials say the death toll from fighting in southern Yemen between army troops and al-Qaida militants has risen to 106, with another 55 soldiers taken prisoner.
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MGH Cancer Center team identifies potential treatment target for KRAS-mutated colon cancerPublic release date: 16-Feb-2012 [ | E-mail | Share ]
Contact: Katie Marquedant kmarquedant@partners.org 617-726-0337 Massachusetts General Hospital
Better understanding of cancer-promoting pathway may lead to new strategy for treatment-resistant tumors
Researchers from the Massachusetts General Hospital (MGH) Cancer Center have identified a new potential strategy for treating colon tumors driven by mutations in the KRAS gene, which usually resist both conventional and targeted treatments. In a paper appearing in the Feb. 17 issue of Cell, the team reports that targeting a later step in the pathway leading from KRAS activation to tumor growth may be able to halt the process.
"Not all KRAS-mutant colon cancers are the same," says Daniel Haber, MD, PhD, director of the MGH Cancer Center and co-corresponding author of the Cell report. "About half seem to be very dependent on the KRAS mutation for their survival, whereas the other half can continue growing even when KRAS is suppressed. In the KRAS-dependent tumors, we identified how the mutation augments a pathway well known to be involved in colon cancer and identified a key step toward that pathway which, if suppressed, can induce KRAS-dependent tumor cells to undergo apoptosis or programmed cell death."
Mutations that activate KRAS expression are common in several types of cancer most frequently colorectal and lung cancers and are known to indicate treatment resistance. Drugs that directly target KRAS activity have not been successful, and attempts to identify other potential targets have been challenging, since KRAS mutations may function differently in different cancers. The MGH team first set out to determine the percentage of KRAS-mutant tumors that depend on the presence of the mutation for their growth.
Analysis of a large panel of KRAS-mutant tumor cell lines revealed that about half of them die when KRAS-expression is blocked. More detailed analysis of the KRAS-dependent tumors identified several overexpressed genes, and found that blocking expression of a growth-factor-associated enzyme called TAK1 was the most effective way of inducing tumor cell death. The researchers then showed that treatment with a TAK1 inhibitor led to the death of cultured KRAS-dependent colon cancer cells and reduced the size of KRAS-dependent tumors implanted under the skin of mice. Further exploration revealed that KRAS activation contributes to tumor development through a pathway involving both TAK1 and the signaling molecule BMP, which serves to augment the Wnt pathway that is known to be involved in both embryonic development and cancer.
"Not all genes that are mutated in cancer can be directly targeted by drugs, but this study shows that if you understand the interrelationships between all the signaling pathways in a particular type of tumor, you may uncover a vulnerability that allows you to bypass the 'undruggable target'," says Haber, who is the Kurt J. Isselbacher/Peter D. Schwartz Professor of Oncology at Harvard Medical School and a Howard Hughes Medical Institute Investigator.
"The TAK1 inhibitor we used in this study is not suitable for human administration, but pharmaceutical companies have small-molecule TAK1 inhibitors which have not yet been developed because their potential application was not clear," Haber adds. "Now we need to establish dosage levels where these or related drugs can work against KRAS-dependent colon cancers without being toxic. Those studies, combined with better understanding of the mechanisms underlying this pathway and the consequences of its suppression, will bring us closer to planning for clinical trials."
###
The lead author of the Cell paper is Anurag Singh, PhD, formerly a postdoctoral fellow at the MGH Cancer Center and now at Boston University's Cancer Research Center. Additional co-authors are Michael Sweeney, Min Yu, MD, PhD, Alexa Burger, PhD, Patricia Greninger and Cyril Benes, PhD, all of the MGH Cancer Center; and co-corresponding author Jeffrey Settleman, PhD, formerly of the MGH and now with Genentech, Inc. The study was supported by grants from the National Institutes of Health and the Lustgarten Foundation.
Massachusetts General Hospital (www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
MGH Cancer Center team identifies potential treatment target for KRAS-mutated colon cancerPublic release date: 16-Feb-2012 [ | E-mail | Share ]
Contact: Katie Marquedant kmarquedant@partners.org 617-726-0337 Massachusetts General Hospital
Better understanding of cancer-promoting pathway may lead to new strategy for treatment-resistant tumors
Researchers from the Massachusetts General Hospital (MGH) Cancer Center have identified a new potential strategy for treating colon tumors driven by mutations in the KRAS gene, which usually resist both conventional and targeted treatments. In a paper appearing in the Feb. 17 issue of Cell, the team reports that targeting a later step in the pathway leading from KRAS activation to tumor growth may be able to halt the process.
"Not all KRAS-mutant colon cancers are the same," says Daniel Haber, MD, PhD, director of the MGH Cancer Center and co-corresponding author of the Cell report. "About half seem to be very dependent on the KRAS mutation for their survival, whereas the other half can continue growing even when KRAS is suppressed. In the KRAS-dependent tumors, we identified how the mutation augments a pathway well known to be involved in colon cancer and identified a key step toward that pathway which, if suppressed, can induce KRAS-dependent tumor cells to undergo apoptosis or programmed cell death."
Mutations that activate KRAS expression are common in several types of cancer most frequently colorectal and lung cancers and are known to indicate treatment resistance. Drugs that directly target KRAS activity have not been successful, and attempts to identify other potential targets have been challenging, since KRAS mutations may function differently in different cancers. The MGH team first set out to determine the percentage of KRAS-mutant tumors that depend on the presence of the mutation for their growth.
Analysis of a large panel of KRAS-mutant tumor cell lines revealed that about half of them die when KRAS-expression is blocked. More detailed analysis of the KRAS-dependent tumors identified several overexpressed genes, and found that blocking expression of a growth-factor-associated enzyme called TAK1 was the most effective way of inducing tumor cell death. The researchers then showed that treatment with a TAK1 inhibitor led to the death of cultured KRAS-dependent colon cancer cells and reduced the size of KRAS-dependent tumors implanted under the skin of mice. Further exploration revealed that KRAS activation contributes to tumor development through a pathway involving both TAK1 and the signaling molecule BMP, which serves to augment the Wnt pathway that is known to be involved in both embryonic development and cancer.
"Not all genes that are mutated in cancer can be directly targeted by drugs, but this study shows that if you understand the interrelationships between all the signaling pathways in a particular type of tumor, you may uncover a vulnerability that allows you to bypass the 'undruggable target'," says Haber, who is the Kurt J. Isselbacher/Peter D. Schwartz Professor of Oncology at Harvard Medical School and a Howard Hughes Medical Institute Investigator.
"The TAK1 inhibitor we used in this study is not suitable for human administration, but pharmaceutical companies have small-molecule TAK1 inhibitors which have not yet been developed because their potential application was not clear," Haber adds. "Now we need to establish dosage levels where these or related drugs can work against KRAS-dependent colon cancers without being toxic. Those studies, combined with better understanding of the mechanisms underlying this pathway and the consequences of its suppression, will bring us closer to planning for clinical trials."
###
The lead author of the Cell paper is Anurag Singh, PhD, formerly a postdoctoral fellow at the MGH Cancer Center and now at Boston University's Cancer Research Center. Additional co-authors are Michael Sweeney, Min Yu, MD, PhD, Alexa Burger, PhD, Patricia Greninger and Cyril Benes, PhD, all of the MGH Cancer Center; and co-corresponding author Jeffrey Settleman, PhD, formerly of the MGH and now with Genentech, Inc. The study was supported by grants from the National Institutes of Health and the Lustgarten Foundation.
Massachusetts General Hospital (www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.
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?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
South Carolina wide receiver Alshon Jeffery was considered a potential top-five pick entering the 2011 college season after an 88-catch, 1,517-yard, nine-touchdown sophomore year. Jeffery?s stats fell to 49 receptions, 762 yards, and eight scores as a junior, and he declared for the draft on January 5.
Jeffery?s supporters cited quarterback musical chairs and defense?s double teams for his 2011 production drop. Appearing on a Wednesday conference call for the media, NFL Network draft guru Mike Mayock said he saw something different.
?Alshon Jeffery does not separate,? said Mayock after watching Gamecocks tape. ?What those guys run [at the Combine] is important. He needs to run somewhere in those mid-4.5s.?
Mayock said he?s heard whispers of Jeffery?s suspect conditioning, rumors that may have begun?with this picture,?believed to have been taken just before the 2011 college season. (Jeffery, No. 1, is on the far left.) For this year?s receiver class, Mayock has first-round grades on Oklahoma State?s Justin Blackmon, Baylor?s Kendall Wright, Notre Dame?s Michael Floyd, and LSU?s Rueben Randle.
He doesn?t have one on Jeffery.
?Big and fast is good,? Mayock explained. ?Big and slow is bad. Bottom line is ? he has got to run well.?
LOS ANGELES ? After days of DNA testimony, prosecutors planned to tell jurors the story of love and betrayal that they claim provided a motive for murder by a veteran police detective.
Witnesses were expected to talk about the personal lives of Stephanie Lazarus and the woman she is charged with killing, retrieving memories of events that happened 26 years ago. Sherri Rasmussen was slain in her home in 1986 three months after she married the man who had spurned Lazarus. Testimony about the love triangle was scheduled for Wednesday.
It comes on the heels of scientific testimony that showed the baffling murder case might have gone unsolved if a forensic analyst had not decided to take a closer look at a single piece of evidence ? a bite mark on the victim's arm.
Until then it appeared this was a cold case with no suspects. Blood at the scene matched the victim but no one else, criminalist Jennifer Francis testified Tuesday. There were literally no leads.
Then, after some five years of working on the case intermittently, Francis said she focused anew on the long ignored bite mark on the victim's arm. She has testified that a saliva swatch from the bite, found in a dusty evidence box, led her to a new theory and a new suspect ? Detective Stephanie Lazarus of the Los Angeles Police Department.
Lazarus showed no reaction in court to the testimony that suggested she might never have been charged with the 1986 murder if the original scientific analysis of blood evidence had gone undisturbed.
Lazarus claims she is innocent of the murder of her onetime romantic rival and her lawyer was trying to show in cross-examination that the prosecution's single important piece of evidence ? the saliva from the bite mark ? may have been tampered with or deteriorated over time.
At one point he asked if the evidence swabs inside a test tube were moldy by the time they got to Francis in the LAPD crime lab.
"It's hard to say," said the witness. "I did not see green growing on it."
He asked if the test tube was sealed, and Francis said it was not.
"So all you had to do was unscrew it?" asked Overland.
"Yes," said the witness.
The bright red bite mark on Rasmussen's arm was shown to jurors on a courtroom screen.
A forensic dentist testified that it appeared to be a human bite mark but Dr. Cathy Law said she did not try to match it to Lazarus' teeth because such comparisons are unreliable.
Witnesses are expected to say that Lazarus was broken hearted when her longtime lover John Ruetten, married Rasmussen. Prosecutors contend the former police detective killed Rasmussen after telling someone if she couldn't have Ruetten then nobody would.
Francis said bloody evidence from the crime scene did not suggest any suspect when she was first given the case in 2004. There was no DNA match for any person other than victim on such items as blood from the walls, a towel, speaker cord and car key, she said.
It wasn't until 2009 that Francis focused on analyzing the bite mark and discovered there was DNA on the sample that was different from the genetic profile of Rasmussen, she said.
Francis testified earlier that the bite mark DNA was subsequently compared to a saliva sample taken from Lazarus' mouth and it was a match.
The discovery shocked Los Angeles Police Department detectives who had worked with Lazarus for a quarter of a century as she rose to become a highly decorated detective specializing in art thefts.
Prosecutors, who are relying on DNA analysis of saliva from the mark, also called a series of forensic witnesses who told how the suddenly important bite mark evidence, previously buried in a dusty evidence box, now was preserved in a freezer, sent to an independent serology lab for further analysis and then returned to the custody of the LAPD crime lab.
In this photo from Wednesday, Feb. 1, 2012, Nicole "Snooki" Polizzi poses for a portrait in New York. Lorena Beniquez, commissioner of the Central Pennsylvania Film Office heard that officials in Hoboken, N.J. have refused to issue a permit for the new reality show that will feature Nicole "Snooki" Polizzi and Jenni "JWoww" Farley. So, Beniquez thought, why not invite the ?Jersey Shore? stars to the borough of the same name, about 140 miles northwest of Philadelphia, and only slightly farther than that from Hoboken. Failing that, Beniquez is hoping the producers might consider shooting in Williamsport, the Lycoming County seat.(AP Photo/Charles Sykes)
In this photo from Wednesday, Feb. 1, 2012, Nicole "Snooki" Polizzi poses for a portrait in New York. Lorena Beniquez, commissioner of the Central Pennsylvania Film Office heard that officials in Hoboken, N.J. have refused to issue a permit for the new reality show that will feature Nicole "Snooki" Polizzi and Jenni "JWoww" Farley. So, Beniquez thought, why not invite the ?Jersey Shore? stars to the borough of the same name, about 140 miles northwest of Philadelphia, and only slightly farther than that from Hoboken. Failing that, Beniquez is hoping the producers might consider shooting in Williamsport, the Lycoming County seat.(AP Photo/Charles Sykes)
HOBOKEN, N.J. (AP) ? An Italian-American group is responding to Hoboken's rejection of MTV's "Jersey Shore" reality show ? by giving the city's mayor an award.
The Italian American One Voice Coalition is presenting Hoboken Mayor Dawn Zimmer with its "Una Voce" award Wednesday for denying film permits to a show the group feels promotes negative stereotypes of Italian Americans.
Zimmer says the decision to deny permits was made based on safety and quality-of-life concerns for residents of Hoboken.
The show has been issued permits to film in Jersey City. The spinoff of the reality series will feature Nicole "Snooki" Polizzi and Jenni "JWoww" Farley renting an apartment in New Jersey's second largest city. Jersey City Mayor Jerramiah Healy says he believes the show is an opportunity to promote the city.
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Public release date: 16-Feb-2012
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