This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Myocardial infarction (MI), or heart attack, can cause long-term damage that leads to heart failure. To treat this type of heart failure, it’s critical to heal the pathological structural changes in the heart and preserve cardiac function. A recent study investigated potential treatment targets by exploring the role of the enzyme ADAM17, whose levels are increased during MI. In a group of 152 patients with MI, high ADAM17 levels were associated with a greater incidence of subsequent heart failure, as well as poorer heart function and higher mortality, suggesting a negative role of ADAM17. In mice with MI, elevated ADAM17 levels were linked to heart damage, but blocking ADAM17 activity limited the cardiac damage and remodeling after MI. Experiments in cultured heart cells revealed that ADAM17 exerted its harmful effects by promoting loss of the cardioprotective enzyme ACE2 and that the activation of ADAM17 depended on modification of a specific site in the protein p38 MAPK..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"More than one-third of people who’ve survived brain hemorrhage stop taking oral anti-blood-clotting drugs, like aspirin. Normally taken to prevent blood vessel blockage, so-called antiplatelet drugs increase the risk of bleeding in general. So they’re widely believed to increase the risk of brain hemorrhage happening again. But new research suggests that might not be the case. Researchers came to that conclusion following a randomized trial involving more than 500 survivors of brain hemorrhage in the UK. Participants were mostly men over the age of 70; all had a history of diseases that cause blockage of blood flow due to clotting but had stopped taking oral antiplatelet drugs after their brain hemorrhage. Researchers split those patients into two groups: half were encouraged to start antiplatelet drugs, and half were encouraged to stay off these drugs..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Reperfusion of heart tissue with blood after interruption of the blood supply (ischemia) often contributes to inflammation and cell death, including a specific form of cell death called pyroptosis, which can be regulated by the protein caspase-4. The protein beclin-1 is involved in an intracellular degradation process called autophagy that can limit cell death. However, whether beclin-1 limits caspase-4-mediated pyroptosis after heart reperfusion injury remains unclear. To find out, a recent study examined the effects of beclin-1 overexpression in mouse hearts and cultured human heart cells subjected to ischemia/reperfusion. Ischemia/reperfusion increased caspase-4 activity and the expression of the pyroptosis protein gasdermin D. In contrast, beclin-1 overexpression decreased caspase-4 activity, gasdermin D expression, and the levels of the inflammation molecule IL-1β..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe the structure of the heart and explain how cardiac muscle is different from other musclesDescribe the cardiac cycleExplain the structure of arteries, veins, and capillaries, and how blood flows through the body

By the end of this section, you will be able to:Describe the structure of the heart and explain how cardiac muscle is different from other musclesDescribe the cardiac cycleExplain the structure of arteries, veins, and capillaries, and how blood flows through the body

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Diabetes is a major risk factor for myocardial infarction, stroke, and other cardiovascular diseases. The prime target for reducing cardiovascular risk is low-density lipoprotein, or LDL. LDL cholesterol has been linked to cardiovascular events in patients with type 2 diabetes. While statins have long been the primary treatment for reducing LDL, many patients are unable to reach recommended levels with a statin alone or are unable to take an effective dose. That places them at an especially high risk for cardiovascular disease. Now, a new study reports the efficacy and safety of evolocumab on top of statins in patients with both type 2 diabetes and hyperlipidemia or mixed dyslipidemia. The double-blind, phase 3 trial was conducted in patients from 10 different countries over a treatment period of 12 weeks. More than 980 patients were randomized to one of four subcutaneous treatments: 140 mg of evolocumab every 2 weeks, 420 mg of evolocumab monthly, or placebo at either of those frequencies..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Background We explore whether the number of null results in large National Heart Lung, and Blood Institute (NHLBI) funded trials has increased over time. Methods We identified all large NHLBI supported RCTs between 1970 and 2012 evaluating drugs or dietary supplements for the treatment or prevention of cardiovascular disease. Trials were included if direct costs >$500,000/year, participants were adult humans, and the primary outcome was cardiovascular risk, disease or death. The 55 trials meeting these criteria were coded for whether they were published prior to or after the year 2000, whether they registered in clinicaltrials.gov prior to publication, used active or placebo comparator, and whether or not the trial had industry co-sponsorship. We tabulated whether the study reported a positive, negative, or null result on the primary outcome variable and for total mortality. Results 17 of 30 studies (57%) published prior to 2000 showed a significant benefit of intervention on the primary outcome in comparison to only 2 among the 25 (8%) trials published after 2000 (χ2=12.2,df= 1, p=0.0005). There has been no change in the proportion of trials that compared treatment to placebo versus active comparator. Industry co-sponsorship was unrelated to the probability of reporting a significant benefit. Pre-registration in clinical trials.gov was strongly associated with the trend toward null findings. Conclusions The number NHLBI trials reporting positive results declined after the year 2000. Prospective declaration of outcomes in RCTs, and the adoption of transparent reporting standards, as required by clinicaltrials.gov, may have contributed to the trend toward null findings.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Heart attacks are dangerous events that lead to a massive loss of heart cells, called cardiomyocytes. The catastrophic damage can be treated by generating cardiomyocytes from stem cells and transplanting them into the heart. The stem cells can then proliferate in the space before becoming new cardiomyocytes by differentiating and maturing. But little is known about how macrophages from the injury site impact stem cell-derived cardiomyocytes. To learn more, researchers cultured these stem cells, called induced pluripotent stem cells (iPSCs), with macrophages of several subtypes. Macrophages start in a non-polarized phenotype (M0) and then can polarize between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. The pro-inflammatory M1 phenotype macrophages were likely to be found at the injury site, and they inhibited iPSC differentiation and maturation..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Heart disease is the leading cause of death worldwide. While people have benefited greatly from advances in drugs and surgery, one glaring problem remains: unlike the cells that make up our other muscles, once heart cells are gone, they simply can’t be regenerated. That is, unless you were just born. Studies show that muscle cells in the hearts of newborn mice, rabbits, and even humans can go on dividing for up to days after birth. And now, in what could be a new world record, scientists have recorded signs of regeneration beyond two weeks after birth in the South American gray short-tailed opossum. Their ability to replicate this feat in mice could point to new ways of healing the hearts of humans with cardiovascular disease. The experiments that led to these results were carried out by Wataru Kimura and colleagues at the RIKEN Center for Biosystems Dynamics Research in Japan..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cardiac fibrosis is tissue scarring that typically follows a heart attack. Growing evidence suggests that this scarring process is mediated by RGS proteins, multifunctional regulators of cell signaling. To better understand how, researchers examined the effects of RGS4, both on in vitro and in vivo models of heart attack. All models showed elevated levels of RGS4, linking the protein to cardiac fibrosis. Silencing RGS4 through RNA interference proved capable of reducing cardiac fibrosis in vitro and in mice. But when overexpressed, RGS4 could counteract the protective effects of choline, a nutrient found in meat that has been shown to reduce cardiac fibrosis. Further experiments revealed that RGS4 exerts its pro-cardiac fibrosis effects through TGFβ1/Smad and MAPK signaling. Future studies will examine how RGS4 interacts with similar proteins to cause cardiac fibrosis, which could lead to new ways of combating the harmful after-effects of heart attack..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"How do you fix a broken heart? According to a new study, TREEs can help—that is, tissue regeneration enhancer elements. The study found that these short DNA control modules from zebrafish can precisely regulate gene expression in mammals to promote healing after a heart attack. Heart attack, or myocardial infarction, and heart failure are common and devastating cardiac conditions. But the hearts of adult mammals can’t regenerate well after injury, making treatment difficult. One option is to attempt to use gene therapy with viral vectors to enhance heart cell proliferation, thus improving cardiac regeneration. However, current gene therapies are limited in their ability to control their cargoes, leading to strong, continuous delivery in one or more organs. And unchecked cell proliferation can lead to problems like tumor formation, making methods for precise control essential. Zebrafish TREEs are promising mediators of such precise control..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Cell death is a hallmark of various abnormalities of the heart, including heart failure, heart attack, and ischemia. While the long-term effects of cell death in the heart have been described, the cellular processes that occur immediately after cell death remain poorly understood. Now, by tracking the movement of calcium ions, researchers are gaining a better idea of what happens right after individual heart cells die. Calcium ions regulate vital cell functions in mammals and therefore serve as a valuable signal of cellular activity and intercell connections. When zapping and killing a single heart muscle cell with a laser, researchers found that different types of surrounding cells responded differently. Nearby myocytes showed a slow and sustained uptick in calcium “sparks,” while distant myocytes were weakly or not affected. This activity was accompanied by mechanical damage in myocytes. Fibroblasts, however, showed rapid shock waves of calcium ion activity..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Heart attacks, or myocardial infarctions, are a major cause of death globally and can leave survivors with severe, lingering symptoms. Exercise is a key rehabilitation tool, but exactly how it helps patients recover is not yet known. The microbes in our gut directly impact our health in other ways, but could they play a role in exercise-related recovery after heart attacks? To test this possibility, a team of researchers used a mouse model of myocardial infarction (MI). First, they demonstrated that exercise training reduced cardiac dysfunction after MI and that exercise after MI altered the gut microbial richness and community structure. Depleting the microbiota prior to MI blocked the protective effects of exercise, suggesting that the benefits were dependent upon the microbiota. Further, transplanting the gut microbiota from exercised post-MI mice conferred cardiac benefits to recipient mice..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Myocardial infarction (MI), also known as a heart attack, is a common but serious cardiac emergency. The severity and mortality of MI are related to overactivation of immune cells called neutrophils. Specifically, excessive activation of a process called neutrophil degranulation appears to impair MI recovery. During degranulation, molecules that can help fight pathogens and repair tissue damage are released from cytoplasmic granules. This is normally beneficial, but too much degranulation can aggravate MI-related injury. Four main types of granules are released: primary/azurophilic, secondary/specific, tertiary/gelatinase, and secretory granules. These granule types are synthesized and released at different times and contain different mixtures of molecules. For example, primary granules contain the enzyme MPO, excess levels of which can impair ventricular healing and function after MI, while secondary granules contain NGAL, which can increase the risk of plaque formation and promote inflammation and fibrosis..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.