Baked Ziti Recipe, Spotlight on Whole Wheat Pasta, Understanding al Dente, How the Nose Fends Off Colds and Fighting Age-Related Muscle Loss
When it comes to comfort food, few dishes can top baked ziti, with its luscious sauce and melted cheeses. And it doesn’t take much effort for all that reward! I’m sharing interesting research that may explain why some people are more prone to colds than others as well as a reminder about maintaining muscle as we age.
Tricolore Soup
Baked ZitiThis delectable dish starts with a rich yet quick tomato sauce. You can substitute a 15-ounce can of diced tomatoes with their juice for the fresh tomatoes but add it after the tomato paste.
Ingredients
- 3 tablespoons extra virgin olive oil, plus more for the baking dish and drizzling
- 2 garlic cloves, chopped
- 1 pound tomatoes, any type, coarsely chopped
- One 6-ounce can tomato paste
- 1 teaspoon sugar
- 1 teaspoon fine sea salt
- 1/2 teaspoon crushed red pepper flakes, plus more to taste
- 1/2 teaspoon freshly ground black pepper
- 1 pound ziti
- 16 ounces ricotta cheese
- 12 ounces mozzarella, thinly sliced
- 1/3 cup freshly grated Parmigiano-Reggiano cheese
Directions
Step 1
Brush a 13-inch by 9-inch baking dish with olive oil; set aside.
Step 2
Heat a medium saucepan over medium heat. When hot, add the 3 tablespoons olive oil and garlic and sauté for 3 minutes, then add the tomatoes. Cook, stirring constantly, until the tomatoes become soft, then push them to the outsides of the pan. Add the tomato paste and cook it until it becomes fragrant and darkens in color, about 5 minutes. Mix the paste with the tomatoes and garlic, then press with a masher to release all of the tomatoes’ juices. Stir in the sugar, salt, and both peppers and continue cooking for 10 minutes.
Step 3
Meanwhile, preheat your oven to 350°F. Cook the ziti according to the package directions until al dente, then drain.
Step 4
Off the heat, stir the ricotta into the sauce, then fold in the pasta. Transfer the mixture to the baking dish. Top with overlapping slices of mozzarella, then sprinkle on the grated cheese.
Step 5
Bake for 25 minutes, until the cheeses are bubbly. Cool for 10 minutes before serving.
Yields 8 servings
Healthy Ingredient Spotlight
Whole Wheat Pasta
To add more nutrients and fiber to your ziti, opt for whole wheat pasta. It’s made from the entire wheat kernel—bran, germ, and endosperm—and retains its vitamins and minerals. While it takes a bit longer to cook, follow package directions to be sure it’s al dente.
Quick Kitchen Nugget
Understanding al Dente
Al dente literally means to the tooth—firm when bitten yet not hard or raw tasting. Most Italian cooks boil pasta to this stage regardless of the recipe. Americans tend to like their pasta more tender. But when it will be twice cooked, as with ziti, lasagna, and stuffed shells, it needs to be al dente before it goes into the oven or else it will be too soft.
If your pasta box doesn’t list al dente cooking time, test a piece about 2 minutes sooner than the general directions and see whether it has a bit of bite. If it’s too firm, check it again in a minute.
For Your Best Health
How the Nose Fends Off Colds
When rhinovirus, the most common cause of the common cold, enters the nasal passages, the cells lining the nose immediately begin working together to fight the infection. These cells activate a wide range of antiviral defenses designed to limit the virus and stop it from spreading. In a study published in the journal Cell Press Blue, researchers show that this early response plays a key role in whether a person becomes sick and how severe their symptoms become. The findings suggest that the body’s reaction to rhinovirus often matters more than the virus itself.
“As the number one cause of common colds and a major cause of breathing problems in people with asthma and other chronic lung conditions, rhinoviruses are very important in human health,” said senior author Ellen Foxman, MD, PhD, of the Yale School of Medicine. “This research allowed us to peer into the human nasal lining and see what is happening during rhinovirus infections at both the cellular and molecular levels.”
To closely observe how nasal cells respond to infection, the research team built a lab-grown model of human nasal tissue with multiple cell types found in the human airway, including mucus-producing cells and cells with cilia, the tiny hairlike structures that help move mucus and trapped particles out of the lungs. “This model reflects the responses of the human body much more accurately than the conventional cell lines used for virology research,” Dr. Foxman said.
Using this model, the researchers were able to monitor how thousands of individual cells respond together during infection. They also examined what happened when the cellular sensors responsible for detecting rhinovirus were blocked. These experiments revealed a powerful defense system coordinated by interferons, which are proteins that interfere with viral entry and replication.
When nasal cells detect rhinovirus, they release interferons that activate antiviral defenses not only in infected cells but also in nearby healthy cells. This coordinated response makes it difficult for the virus to reproduce and spread. If interferon activity begins quickly, the infection can be contained early. When the researchers blocked this response, the virus spread rapidly, infecting many more cells and causing significant damage. In some cases, the infected organoids did not survive.
“Our experiments show how critical and effective a rapid interferon response is in controlling rhinovirus infection, even without any cells of the immune system present,” said first author Bao Wang, PhD, of the Yale School of Medicine.
The study also uncovered additional responses that occur when viral replication increases. Under these conditions, rhinovirus can activate a separate sensing system that leads both infected and uninfected cells to produce large amounts of mucus and inflammatory signals. This reaction can contribute to airway inflammation and breathing difficulties in the lungs. According to the researchers, these pathways may offer useful targets for treatments aimed at reducing harmful symptoms while supporting effective antiviral defenses.
“Our study advances the paradigm that the body’s responses to a virus, rather than the properties inherent to the virus itself, are hugely important in determining whether or not a virus will cause illness and how severe the illness will be,” Dr. Foxman said. “Targeting defense mechanisms is an exciting avenue for novel therapeutics.”
Fitness Flash
Fighting Age-Related Muscle Loss
A new study in mice is giving scientists fresh clues about why our muscles lose strength as we get older and why exercise remains one of the most reliable ways to fight it.Researchers at Duke-NUS Medical School found that a gene regulator called DEAF1 seems to push a key muscle-maintenance system into overdrive as we age. When we’re young, the system known as mTORC1 helps build and repair muscle. But later in life, it can get stuck in high gear and begin to damage muscle cells instead.
“The mTORC1 pathway is essential for muscle growth yet becomes chronically overactive in aging—a paradox that has made it challenging to pinpoint what drives this dysregulation,” said the study’s senior author Hong-Wen Tang, PhD, an assistant professor in the Cancer and Stem Cell Program at Duke-NUS and Singapore General Hospital.
Until now, scientists didn’t know what caused this shift. “Identifying DEAF1 fills an important gap in understanding how age-related stress signals become hardwired into a persistent anabolic state that ultimately harms muscle cells,” Dr. Tang said.
The study suggests DEAF1 essentially hits the gas on a system already running too fast. By pushing mTORC1 into overdrive, DEAF1 causes muscles to make too many proteins, fail to clear damaged ones, and gradually weaken.
One of the most surprising findings: Exercise reverses this process by lowering DEAF1 levels. That means in addition to building muscle, physical activity helps reset the core cellular pathways that keep muscles healthy. “It was a striking discovery,” said Dr. Tang. “It shows that exercise doesn’t just fix damage; it targets the switch that causes muscle aging in the first place.”
Scientists didn’t just look at whether exercise keeps muscles strong—they wanted to know how it does it. They put aging mice through endurance workouts, including an exhausting treadmill run. For comparison, another group of older mice stayed sedentary. After the workouts, the exercising mice showed big drops in mTORC1, the overactive pathway linked to muscle loss and function known as sarcopenia.
Researchers found that exercise lowers DEAF1 through a well-known set of longevity genes called FOXO. When activated during exercise, FOXO suppresses DEAF1—lifting the foot off the gas pedal—and helps mTORC1 return to normal. Their work highlights a new biological pathway—the FOXO-DEAF1-mTORC1 axis—that helps explain why muscles weaken with age and why exercise remains such a powerful antidote to age-related decline.
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