Archive for the ‘Science’ Category
Sunday, February 12th, 2017
This essay is a response to the hand wringing of many academic and corporate medical workers lamenting the potential effect of the recent travel ban, which was blocked in a most absurd and unconstitutional manner by a 3-judge panel of the 9th circuit court of appeals.
Travel Ban is Revealing ––––but Does Not Threaten American Medicine
Jane Orient, M.D.
A 90-day ban on travel from seven countries has sparked tremendous outpourings of “worry” or outright opposition by some 33 medical organizations.
“The community is reeling over the order, fearing that it will have devastating repercussions for research and advances in science and medicine,” states an article in Modern Healthcare.
Certainly the order is disrupting the lives of individual physicians who have won coveted positions in American medical institutions and were not already in the U.S. when the order was issued. Also their employers have a gap in the work schedule to fill. War tears people’s lives apart, however innocent they may be. And countries that sponsor terrorism have effectively declared war on the U.S.
But is American medicine so fragile that it can’t survive a 90-day delay in the arrival of physicians, most of them trainees, from Iran, Iraq, Libya, Syria, Yemen, Somalia, and Sudan? After all, every year more than a thousand seniors in U.S. medical schools do not land a position in a post-graduate training program through the annual computerized “Match” of graduates with internships. After another chance through the Supplemental Offer and Acceptance Program, or SOAP, hundreds of seniors are still without a job. This means that they cannot get a license to practice in the U.S., however desperate rural communities or inner-city hospitals are to find a physician, and their four years of rigorous, costly post-college education are wasted. Yet James Madara, CEO of the American Medical Association (AMA), is worried about vacant residency slots, according to a Feb 3 article in MedScape by Robert Lowes.
Entry to medical school is highly competitive, so presumably all the students are well-qualified. Can it be that graduates from Sudan are better trained? Does the U.S. have so few young people capable of and interested in a medical career that we have to depend on a brain drain from countries that are themselves desperately short of physicians?
For all the emphasis on “cultural competence” in American medical schools, and onerous regulations regarding interpreters for non-English speakers, what about familiarity with American culture and ability to communicate effectively with American English speakers? Some foreign-born graduates are doubtless excellent, but many American patients do complain about a communication gap. So why do some big institutions seem to prefer foreigners? Could it be that they want cheap, and above all compliant labor? Physicians here on an employment-related visa dare not object to hospital policy.
Whatever the reasons for them, here are some facts about the American medical work force:
- One-fourth of practicing physicians in this country are international medical graduates (IMGs), who are more likely to work in underserved areas, especially in primary care, according to Madara.
- According to the Accreditation Council for Graduate Medical Education (ACGME), 10,000 IMGs licensed in the United States graduated from medical schools in the seven countries affected by the ban.
- Immigrants account for 28% of U.S. physicians and surgeons, 40% of medical scientists in manufacturing research and development, and 15% of registered nurses, according to the Institute for Immigration Research at George Mason University. More than 60,000 of the 14 million workers in health-related fields were from the seven countries affected by the ban.
Is medicine, like agriculture, now filled with “jobs that Americans won’t do”? Actually, we have more than enough Americans who love medical work. But some of best doctors are being driven out by endless bureaucratic requirements, including costly “Maintenance of Certification™” programs that line the pockets of self-accredited “experts” but contribute nothing to patient care. They are being replaced (substituted for) by “mid-levels” with far less training. Then there are thousands of independent physicians having to retire or become employees because they can’t afford the regulatory requirements—soon to be greatly worsened by MACRA, the new Medicare payment system. Physician “burnout” is becoming so bad that we lose up to 400 physicians—the equivalent of a large medical school class—to suicide every year.
The U.S. should be a beacon to attract the best and brightest, and it should welcome those who want to become Americans. Unfortunately, the lives of Americans, as well as the opportunities of aspiring foreign-born doctors, are threatened by those who desire to kill Americans and destroy our culture. These must be screened out.
Meanwhile, the reaction of organized medical groups to the travel ban is spotlighting serious problems in American medicine.
Jane M. Orient, M.D.obtained her undergraduate degrees in chemistry and mathematics from the University of Arizona in Tucson, and her M.D. from Columbia University College of Physicians and Surgeons in 1974. She completed an internal medicine residency at Parkland Memorial Hospital and University of Arizona Affiliated Hospitals and then became an Instructor at the University of Arizona College of Medicine and a staff physician at the Tucson Veterans Administration Hospital. She has been in solo private practice since 1981 and has served as Executive Director of the Association of American Physicians and Surgeons (AAPS) since 1989. Dr. Orient is the 2017 recipient of The Edward Annis award for medical leadership.
Friday, January 27th, 2017
A most interesting article attempting to explain the destruction of the dinosaurs. If correct, we better hurry up and build all those space ships necessary to get us out of here soon, or in the far future, when the next asteroid comes our way.
Lights Out:Asteroid Triggered Freezing Darkness That Killed Dinos
By:Laura Geggel, Senior Writer
The study was published online Jan. 13 in the journal Geophysical Research Letters. Original article on Live Science.
When a giant asteroid careened into Earth about 66 million years ago, the enormous collision led to the formation of an airborne “curtain” of sulfate molecules that blocked the sun’s light and led to years of freezing cold and darkness, a new study finds.
The finding shows how these droplets, or aerosols, of sulfuric acid formed high in the atmosphere, and likely contributed to the deaths of 75 percent of all animals on Earth, including nonavian dinosaurs such as Tyrannosaurus rex and long-necked sauropods, the researchers said.
Earlier studies suggested that the dino-killing asteroid kicked up dust and debris that hung in the air and blocked sunlight in the short term. But by using computer simulations, the researchers of the new study showed how droplets of sulfuric acid contributed to long-term cooling. [Wipe Out: History’s Most Mysterious Extinctions]
Moreover, the sudden, drastic drop in temperature likely caused the surface of the oceans to cool, which would have massively disturbed the marine ecosystems, the researchers said.
“The big chill following the impact of the asteroid that formed the Chicxulub crater in Mexico is a turning point in Earth history,” the study’s lead researcher Julia Brugger, a climate scientist at the Potsdam Institute for Climate Impact Research (PIK) in Germany, said in a statement. “We can now contribute new insights for understanding the much debated ultimate cause for the demise of the dinosaurs at the end of the Cretaceous era.”
Brugger and her colleagues employed a type of computer simulation typically used for climate modeling. The model showed that gases containing sulfur evaporated during the violent impact. These sulfuric molecules were the main ingredients that blocked the sun’s light on Earth and led to plummeting temperatures, they said.
For instance, before the asteroid hit, the tropics were an average temperature of 81 degrees Fahrenheit (27 degrees Celsius). But after the massive impact, the average temperature was 41 F (5 C), the researchers said,”It became cold, I mean, really cold,” Brugger said. Globally, temperatures fell at least 47 F (26 C). For at least three years following the asteroid’s crash, the average annual temperature fell below freezing, and the polar ice caps grew in size.
“The long-term cooling caused by the sulfate aerosols was much more important for the mass extinction than the dust that stays in the atmosphere for only a relatively short time,” study co-researcher Georg Feulner, a climate scientist at PIK, said in the statement. “It was also more important than local events like the extreme heat close to the impact, wildfires or tsunamis.”
In all, it took 30 years for Earth’s climate to recover, the researchers said.
As the air cooled, so did the ocean’s surface waters. This cold water became denser and thus heavier, and sank into the depths of the ocean. Meanwhile, warmer water from the deeper ocean rose, bringing up nutrients that likely led to giant algal blooms, the researchers said.
It’s possible these algal blooms produced toxic substances that affected life along the coasts, the researchers said. But regardless of whether they were toxic or not, the ocean’s massive mixing would have disrupted the marine ecosystem, and likely contributed to the extinction of its species, including the ammonites and the reptilian sea beasts known as plesiosaurs.
The new research illustrates what might happen to Earth if another asteroid were to cross its path, the researchers said.“It is fascinating to see how evolution is partly driven by an accident like an asteroid’s impact — mass extinctions show that life on Earth is vulnerable,” Feulner said. “It also illustrates how important the climate is for all life-forms on our planet. Ironically today, the most immediate threat is not from natural cooling but from human-made global warming.”
Tuesday, January 17th, 2017
The following is a most interesting article about aging, immortality, and what the future might hold for humanity. It’s a must read.
THE HUFFINGTON POST
On the Verge of Immortality, Or Are We Stuck with Death? A New Direction For Research Could Provide the Answers—and More
Bernard Starr, PhD
How long can human beings live? Is there an outside limit? Do we know enough about aging to break through possible biological barriers? Is the current approach to curing “age associated diseases” like Alzheimer’s flawed? Experts are sharply divided.
In 1962 eminent biologist Leonard Hayflick discovered that normal human fetal cells replicate a limited number of times. This phenomenon promptly acquired the moniker the “Hayflick Limit.” Later, biologists Calvin Harley and Carol Greider provided the molecular explanation for the Hayflick limit with their discovery that telomeres, the DNA biological material in every cell of our bodies, diminish each time cells divide.
In contrast, cancer cells, which are immortal, produce an enzyme called telomerase that maintains the length of telomeres and enables cancer cells to replicate without limit. The strategy of extending the life of normal cells by injecting telomerase has proven thorny, as reported by Dr. Elizabeth Blackburn, co-discoverer of telomerase: “too much telomerase can help confer immortality onto cancer cells and actually increase the likelihood of cancer, whereas too little telomerase can also increase cancer by depleting the healthy regenerative potential of the body..telomerase shots are not the magical anti-aging potion….”
The finite capacity of normal human fetal cells to divide (on average about 50 times) suggested to Hayflick that aging is responsible for the end of normal cell replication and eventually death. Other researchers translated Hayflick’s findings into a maximum human lifespan of 120 years.
A 2016 study at the Albert Einstein School of Medicine came up with a similar human lifespan limit of 115 years. The investigators drew their conclusion from surveys of longevity and mortality records in more than forty countries since 1900. While their findings showed an impressive increase in the number of people living beyond age 100 in recent decades, rarely did centenarians live longer than 115 years. One exception, Frenchwoman Jeanne Calment, died at age 122. She was a media sensation because she exceeded the traditional limit for longevity.
The dramatic increase in life expectancy from 18 years (at birth) in prehistoric times to an average of 79 in the U.S. today (and 1-4 years longer in more than 25 other countries) is not due to breakthroughs in our understanding of the biology of aging. Rather, it’s been achieved through the reduction in infant mortality, public health measures such as clean water, improved sanitation, better nutrition, healthy life styles, and the remarkable boost when antibiotics and vaccines were introduced.
But is the Hayflick Limit fixed, or is it a biological barrier that can be penetrated? Opinions vary.
At one extreme, Cambridge University trained Dr. Aubrey de Grey, Chief Science Officer of the SENS Research Foundation for the study of aging claims that emerging breakthroughs in the biology of aging have brought human lifespan to the verge of vastly extended longevity—and perhaps immortality. The first person to live to 1,000 years is likely walking the earth right now, he declares.
I met Aubrey de Grey several years ago at a screening of the film To Age or Not To Age, sponsored by the International Longevity Center. He was one of the researchers featured in the documentary. Afterwards I approached him with a question.
“Do you think civilization is ready for immortality?” I asked, since immortality has obvious implications for the social, economic, and political functioning of society.
De Grey didn’t like my question. He immediately launched into a lengthy rant. “Do you know how many people die each day and that it’s not necessary,” he remarked. “We have the means and knowledge…” I quickly realized that de Grey champions another version of right to life. So sure is he that death is not inevitable that he recoils at the idea that we dare think otherwise.
Dr. Leonard Hayflick takes a strong stand against De Grey’s position on life extension. And he has little respect for those touting “cures for aging.” The “fountain of youth” business, he says, is the first or second oldest profession.
What does Hayflick think of the work of MIT biologist Dr. Leonard Guarente I wanted to know. In 2016 Guarente generated a lot of fanfare when his newly formed company, Elysium, introduced a nutritional supplement called Basis. The main ingredient of Basis, nicotinamide riboside (NR), raises the body’s levels of nicotinamide adenine dinucleotide (NAD), which in turn, Guarente claims, can slow the aging process by boosting mitochondria, the energy dynamo of cells that diminishes with age. While Guarente’s Basis and anti-aging products of other companies may improve some aspects of bodily functioning, do they put the brakes on aging? Hayflick is doubtful if not dismissive of that notion.
I interviewed Dr. Hayflick on the telephone on October 27th and 29th 2016. He spoke from his home in Northern California. The strength of his voice, not to mention his convictions, belie his eighty-eight years. And he anticipates many productive years ahead, based on the principle that the best way to insure longevity is to pick your parents carefully. His mother lived to 106.
While he agrees that biology plays a role in longevity, Hayflick rejects claims that a genetic aging code is about to be broken, thus opening the floodgates for unlimited lifespans. In stark contrast to those who argue that researchers have accumulated a trove of knowledge about aging, Hayflick insists that “We know very little if not zero about the fundamental cause of aging.”
He emphasizes that all the advances in average life expectancy that have been derived from prevention and cures for diseases have not told us anything about the fundamental etiology of aging. “We do not know why cells age,” Hayflick told me. And until we expand our knowledge of the fundamental cause of aging he does not foresee significantly extending average life expectancy; he is even less hopeful about extending human lifespan beyond the current limit.
Hayflick says that if cures are miraculously found for the leading causes of death, that will add about 13 years to average life expectancy. But, he points out, those cures will not increase the lifespan beyond the current limit. He warns: “People will continue to die as a result of aging.” The explanation for why they are dying, he insists, will only be found by unraveling the mystery of the cause of molecular and cellular aging.
“How likely is that to happen?” I asked him. “Very unlikely,” he admitted. Hayflick laments that two to three percent at most of the $1.27 billion that the National Institute of Aging (NIA) spends annually on aging research is allocated to fundamental biological research. That’s why “little work is being done on the basic understanding of aging—not only in this country but worldwide.”
According to Transparency Market Research, the anti-aging market is projected to reach $91.7 billion globally by 2019. Most of that money will be for anti-aging products and services with possibly only a tiny percentage for basic biological research.
Dr. Jan Vijg, Chair in Molecular Genetics at the Albert Einstein School of Medicine in New York City, and a lead researcher on the recent longevity study, confirmed in an interview on November 16, 2016, that a miniscule amount of funding goes to basic biological research, where many of the questions about aging are more likely to find answers. Vijg agrees with Hayflick about the dearth of knowledge about cellular aging. He says we know a lot about factors such as genomes (the DNA of genes) that affect cellular senescence but the question of why cells age remains largely unanswered.
On the positive side, Vijg notes that scientists in the field of aging are increasingly focusing on the biology of aging, not just the cure of diseases. He told me that he has recently applied for a large grant for the study of drugs that target aging rather than specific diseases. Hayflick, he acknowledges, “was the original defender of this position to study aging per se and now he’s been proven correct.”
If that direction is endorsed by a growing consensus of scientists, why the dearth of funding, I asked?
Dr. Vijg points to an entrenched establishment driven by the public, special interests, and lobbyists who want immediate results. People accept aging and death as natural facts of life, Vijg says, but they don’t accept diseases as natural and thus they want cures for them. Basic research may seem abstract and remote. Few laypeople grasp that unraveling the underlying biology of aging could produce faster and more successful results.
Token funding for basic research on the biology of aging makes no sense, Hayflick argues, when it’s clear that aging is the condition that increases vulnerability to age-associated diseases. Physicians and other experts on aging talk glibly, he says, about age-associated diseases such as cancer, cardiovascular, Alzheimer’s, and other illnesses for which the elderly are at greater risk. And then they immediately utter the mantra that the greatest risk factor for age-associated diseases is aging. “But,” he adds, “they never ask themselves why all these major causes of death are occurring in older people.” If you try to answer that question logically, he continues, “you come to the conclusion that there must be something in old cells that provides the milieu or the opportunity for age-associated diseases that does not occur in young cells.” Isn’t it therefore highly probable, he conjectures, that “old cells may provide the condition that allows for the emergence of all age-associated diseases?”
If Hayflick’s analysis is correct, shouldn’t a significant part of the fifty percent of the NIA budget for aging research, which Hayflick says is designated for the treatment and cure of Alzheimer’s (Vijg estimates an even higher percentage), be shifted to research on molecular and cellular aging, where a cure may be found?
Hayflick gets emotional in his frustration that researchers are not aggressively pursuing a strategy to understand why old cells are different from young cells: “Why in the hell aren’t we studying the fundamental biology of aging if that is the major risk factor for age-associated diseases? Why are we ignoring it almost 100 percent?”
While unlocking the keys to cellular aging might enable vast numbers of people to live closer to the limit of life expectancy, Hayflick still cautions that it will not extend lifespan beyond its current limit. What then does he say about the limit? Is it fixed or can it be extended. And if it is possible to increase it, by how much?
Here Hayflick’s analysis turns to an overarching law of nature. He explains that cells, like all things animate and inanimate, are subject to the second law of thermodynamics, which states that energy dissipates or spreads out when not constrained. Applied to aging, this means that entropy (energy dissipation) increases over time—and the increase in entropy forecasts the inevitability of death. Sounds pessimistic, but is that the end of the story? Maybe not.
Vijg acknowledges entropy as a limiting factor, but he believes it could be slowed if we had a better understanding of entropy at the cellular level. He also expresses great faith in science and therefore will not rule out future discoveries that could lead to a significant increase in human lifespan. Hayflick as well will not bet against science, but he adds this stern caveat: “First we must invest substantially in the study of the basic biology of aging.”
Note: The first and second laws of thermodynamics were introduced by Rudolf Clausius and William Thomson around 1850.
Bernard Starr,PhD, is Professor Emeritus at the City University of New York (Brooklyn College), where he directed a graduate program in gerontology. He is founder and editor of a number of publications in the field of aging: The Springer Publishing Company Series on Adulthood and Aging, the Springer Series on Lifestyles and Issues in Aging, and the cutting edge Annual Review of Gerontology and Geriatrics. For seven years he was writer, producer and host of an award winning radio commentary, The Longevity Report, on WEVD-AM Radio in NYC. During the same period— for three years—he wrote op-ed articles for the Scripps Howard News Service on healthcare, the “boomers,” and issues of an aging society.
Follow Bernard Starr on Twitter: www.twitter.com/starrprobe
Leonard Hayflick has studied the fundamental biology of aging for over 50 years. He discovered that cultured normal human cells are mortal and age and that only cancer cells are immortal thus upsetting a 60-year old dogma.
Hayflick is a Fellow of the American Association for the Advancement of Science, an Honorary Member of the Tissue Culture Association and, a Life Member of the British Society for Research on Ageing. According to the Institute of Scientific Information, he is one of the most cited contemporary scientists in the world “in the fields of biochemistry, biophysics, cell biology, enzymology, genetics and molecular biology.” Dr. Hayflick is the author of over 280 scientific papers, book chapters and edited books of which four papers are among the 100 most cited scientific papers of the two million papers published in the basic biomedical sciences from 1961 to 1978.
Dr. Hayflick is the author of the popular book, “How and Why We Age” published in August 1994 by Ballantine Books, NYC and available in 1996 as a paperback. This book has been translated into nine languages and is published in Japan, Brazil, Russia, Spain, Germany, the Czech Republic, Poland, Israel and Hungary. It was a selection of The Book-of-the-Month Club and has sold over 50,000 copies world-wide.
Monday, December 12th, 2016
When I was first in the practice of cardiology, a heart attack was a fearsome problem. Our tools for handling it were primitive especially in light of what we know about the process and its management with today’s technology. Over the years, the understanding of coronary artery disease, coronary thrombosis, lipids, etc. have blossomed along with a greater and greater sophistication in dealing with a heart attack. In addition, with time, research, and the burgeoning of our tools, the understanding of the variability in the presentation of heart attacks have led to an increased capability in handling such cases.
Despite our new technology, a major element in cardiac diagnosis for over a century has been, and still is, the electrocardiogram invented in 1903 by Willem Einthoven, a Dutch physiologist. It remains today a critical tool in much of cardiology, including in the diagnosis and management of heart attacks. The alterations in the EKG during a heart attack can help assess the possible severity of the attack and possibly the prognosis.
What exactly is a STEMI Heart Attack?
A STEMI is a full-blown heart attack caused by the complete blockage of a heart artery. A STEMI heart attack is taken very seriously and is a medical emergency that needs immediate attention. STEMI stands for ST elevation myocardial infarction. “ST elevation” refers to a particular pattern on an EKG heart tracing and “myocardial infarction” is the medical term for a heart attack. So STEMI is basically a heart attack with a particular EKG heart-tracing pattern.
When someone is being evaluated for chest pain the EKG tracing is done as soon as possible to help see if it’s the heart. An ST-elevation myocardial infarction (STEMI) is a combination of symptoms of chest pain and a specific STEMI EKG heart tracing. The EKG has to meet what is called STEMI criteria to make a correct diagnosis, just like an NSTEMI will provide another set of specific diagnostic criteria. The EKG also provides information as to which part of the heart the blocked artery is supplying, for example an anterior vs. a posterior STEMI vs. an inferior STEMI. An anterior STEMI is the front wall of the heart, and the most serious. A posterior STEMI is the back wall of the heart. An inferior STEMI is the bottom wall of the heart.
What Happens to the Heart?
In a heart attack there is sudden rupture of an unstable part of the wall in a heart artery (coronary artery). This leads to a build up of clot in an attempt to heal it. However this clot formation results in total blockage of the artery. Unfortunately, this total blockage leads to loss of blood supply to the heart beyond that point. The heart muscle stops working within minutes of this and dies within minutes to hours unless the artery can be opened up and illustrates what is the primary goal in tratment –––– to rescue as much heart muscle as possible. For this reason every minute from the onset of a heart attack is absolutely critical. Often the patient doesn’t make it to the hospital due to sudden death due to a malignant heart rhythm. For those that leave it too long to get help or for those in whom the heart attack isn’t treated, the heart muscle dies and is replaced by a non beating scar.
The most important part of any STEMI treatment protocol is to get to the hospital as quickly as possible, so basically to call 911 immediately!!! In a STEMI, an artery is blocked and treatment centers on opening this up as quickly as possible. The preferred way to do this is by performing something known as an angioplasty and stent placement. In this procedure the artery is opened up working through a small tube passed into the heart either from the wrist or the groin. In some cases this cannot be performed quickly enough (less than 90-120 minutes) because of being too far away from a hospital equipped to do these things, and in order to avoid a significant delay in any treatment, clot busting drugs are used. Unfortunately these clot busters are not as good since they are less likely to open the artery and are also associated with bleeding complications. However, they are better than no treatment at all. So sometimes we have to use them.
In addition to this, a number of other treatments are used. Painkillers such as morphine are required to settle down pain and reduce anxiety. Oxygen is administered to those who are breathless or have heart failure. EKG monitors are attached so that potentially lethal arrhythmias such as ventricular fibrillation or even less dangerous but still significant arrhythmias such as inappropriate sinus tachycardia or atrial fibrillation with a rapid heart rate can be identified and treated. Blood thinners such as heparin, aspirin and other platelet inhibitors (clopidogrel/ticagrelor) are used to improve outcomes and prevent more heart attacks.
Educating patients and their families is one of the most critical aspects of care after a STEMI. Several new medicines are started after a heart attack, several of which may be needed lifelong. Patients need to be sure they take the medications prescribed to have a benefit. I’ll address these briefly later. Stopping smoking is essential. It’s important patients follow up with their doctors. Drugs should be used to control blood pressure. After a STEMI patients will be enrolled in cardiac rehabilitation that is a program they should attend on a regular basis. This involves exercise, addressing questions such as time of return to physical activities and dietary concerns. Following these things after the STEMI is arguably as important as treating the STEMI itself.
What exactly is a Non-STEMI Heart Attack
As previosly indicated, ST refers to the ST segment, which is part of the EKG heart tracing used to diagnose a heart attack. NSTEMI stands for Non-ST segment-elevation myocardial infarction. Nevertheless, a NSTEMI is still a type of heart attack, although presenting in a somewhat less acute manner than a STEMI. A myocardial infarction is, of course, the medical term for a heart attack.
How is a NSTEMI diagnosed?
In addition to signs such as chest pain, a heart attack is diagnosed mainly two ways. First is a blood test that shows elevated levels of certain markers of heart damage such as cardiac troponin. Secondly is by looking at the EKG heart tracing. As we have already shown, if there is a pattern known as STsegment-elevation on the EKG, this is called a STEMI, short for ST elevation myocardial infarction. If there is elevation of the blood markers suggesting heart damage, but no ST elevation seen on the EKG tracing, this is known as a NSTEMI, a non ST segment elevation myocardial infarction. A NSTEMI may be associated with other EKG changes such as ST segment depression. Often looking at the EKG helps us to locate the area of the heart that is affected.
Treatment of Non STEMI Myocardial Infarction
In addion to the EKG, part of the way of diagnosing a NSTEMI is by a blood test called troponin that is indicative of heart damage. Although the troponin test is great in that it does not miss heart attacks, it is not specific for heart attacks alone. Once the patient’s problem is diagnosed as a NSTEMI, the treatment strategy will typically include an echocardiogram to look at heart muscle functioning. Initially, blood-thinning agents will be given such as aspirin and the blood thinner heparin. These medicines have been proven to improve outcomes in patients with NSTEMI. There may be other medicines given such as a beta-blocker or nitrates. Many patients will then go for a heart catheterization. This test involves injecting dye into the heart arteries to look for blockages. In the case of severe blockages, treatment in the form of a stent or multiple stents may be required. Sometimes there are so many blockages that bypass surgery is advised.
Prognosis after a NSTEMI
A NSTEMI IS a heart attack, so the treatment of that applies here as well. Medicines are prescribed that have been proven to save lives in the long term for heart attack sufferers. Depending on factors such as symptoms and heart function, a number of medicines may be prescribed. Lifestyle changes and modification of risk factors are key in preventing recurrence. It is important for smokers to stop smoking. Blood pressure control and control of diabetes are key. A post-heart attack exercise plan should be incorporated into a daily lifestyle if possible. Often NSTEMI patients will be sent to cardiac rehab to receive education on the important of exercise and begin a program in a supervised environment.
Common Medicines Prescribed After a Non STEMI or STEMI Myocardial Infarction
Aspirin, antiplatelet agents, Beta-Blockers, ACE-Inhibitors and Statins are often prescribed.
STEMI vs NSTEMI – Which is Worse?
The bottom line is that both are bad. STEMI is seen as more of an immediate emergency because there is a known total occlusion of a heart vessel that needs opening urgently. In terms of long-term outcomes, they have equal health implications. Patients with NSTEMI often have other illnesses such as ongoing critical illness, diabetes, kidney disease, and other that means they have a generally high risk over the long term. Both STEMI and NSTEMI need aggressive treatment over the short and long term.
Monday, December 12th, 2016
This is a magnificent article on a most astonishing force of nature and helps point out how infintely infinitessimal we all are, even our Milky Way Galaxy, in this strange Universe in which we survive for less than a micromillisecond of time.
Super Spiral Galaxies Amaze Astronomers
A new breed of giants raises questions about how the biggest galaxies arise
By Ken Croswell on December 8, 2015
Sporting a double nucleus, the super spiral galaxy CGCG 122-067 in the constellation Leo emits roughly eight times as much visible light as the Milky Way.
They’re big, they’re bright, they’re beautiful—and they shouldn’t even exist, at least to our current astronomical knowledge: gargantuan spiral galaxies that make our giant Milky Way seem downright modest. Spirals are supposed to be small fry compared to the greatest giant ellipticals, which are football-shaped swarms of stars thought to be the universe’s biggest and brightest galaxies. But now a search across billions of light-years has snared a rare breed of “super spiral” galaxies that rival their giant elliptical peers in size and luminosity, raising questions over how such behemoths are born.
“I was really surprised,” says Patrick Ogle, an astronomer at the California Institute of Technology who discovered the super spirals earlier this year. Ogle looked for them by analyzing the NASA Extragalactic Database, an online compendium of galaxy information. He examined nearly 800,000 galaxies within 3.5 billion light-years of Earth, ranking them by luminosity—in particular, by how much visible light they radiate. Astronomers designate the characteristic luminosity of big galaxies with the symbol L*, which is pronounced “L star” and roughly corresponds to the brightness of our own Milky Way.
Galaxies much brighter than L* are extremely rare, and are typically ellipticals. Nevertheless, such powerhouses do exist, and the brightest galaxy in Ogle’s sample shone with a luminosity of 20 L*. Sure enough, it was a giant elliptical galaxy in a galaxy cluster.
But as Ogle’s team reports in work submitted to The Astrophysical Journal last month, three percent of the most luminous galaxies they found are actually spirals. “They look like normal spiral galaxies, but until you quantify how far away they are, you don’t realize how big and bright they are,” Ogle says. “I think that’s probably why people didn’t notice them before.” His sample shows 53 spiral galaxies with luminosities between eight and 14 L*. The largest super spiral, located in the constellation Hercules, possesses a disk of stars 440,000 light-years across, four times the size of the Milky Way’s stellar disk.
“These things are really rare,” Ogle says. Super spirals only pop up once in every billion cubic light-years of space, so astronomers have to look a long way to see any. Whereas the best-known giant elliptical galaxy, M87 in the Virgo cluster, is 54 million light-years from Earth, the closest super spiral galaxy in Ogle’s sample is 1.2 billion light-years distant. Because of their great distance, these galaxies look blurry in current images; the Hubble Space Telescope has not yet imaged them to reveal their full beauty.
William Keel, an astronomer at the University of Alabama, Tuscaloosa who was not affiliated with the research, says he knows of only one remotely comparable galaxy: the equally large but less luminous UGC 2885, a spiral galaxy in the constellation Perseus. “One [galaxy] is a pet rock; ten is a statistical sample,” Keel says. With more than fifty super spirals now known, astronomers hope to learn how these enormous entities arose.
“That’s the biggest puzzle,” says Debra Elmegreen, an astronomer at Vassar College not involved with the discovery of the super spirals. “Why are they there? Why aren’t they already ellipticals?” Elliptical galaxies can grow huge because they often occupy the busy centers of galaxy clusters, where they gobble other galaxies. Spiral galaxies prefer quieter, less populous neighborhoods; moreover, galactic collisions usually disrupt the delicate spiral galaxies and transform them into amorphous ellipticals.
Still, even normal-sized spiral galaxies can outshine their giant elliptical counterparts in star formation, which mostly occurs in a spiral galaxy’s gas-and-dust-packed arms. The super spirals are no exception, and are prodigiously producing stars by converting between five and 65 solar masses of gas into suns each year. For comparison, the Milky Way’s rate is just two solar masses a year. Spirals can sustain their star-making over eons by grabbing additional gas from intergalactic space. As a galaxy grows more massive, however, that infalling gas crashes in so fast it heats up to tremendous temperatures that inhibit star formation. So a spiral galaxy should only get so big. Yet, somehow, the super spirals keep on growing.
One clue to their origin may come from the finer details of their architecture. Four out of fifty-odd super spirals have double nuclei, suggesting that each of the four arose from the merger of two smaller spiral galaxies. Normally a spiral-spiral merger makes an elliptical galaxy, but if two spirals approach each other just right—with their disks parallel and both spinning the same direction—the pair can join forces to create an even larger spiral galaxy. In support of this idea, two of the super spiral galaxies harbor bright quasars at their centers. A quasar lights up when gas plummets into a galaxy’s central supermassive black hole, a process often triggered by a galactic merger.
Ogle says the super spirals will eventually fade over billions of years as they run out of gas and cease star formation. He suspects each will become a so-called lenticular galaxy, a cross between a spiral and an elliptical: Like a spiral galaxy, a lenticular has a disk of stars, but like an elliptical galaxy, it has too little gas to give birth to any more, and lacks spiral arms. Long before the super spirals suffer this fate, however, an armada of telescopes is sure to scrutinize them to settle once and for all how these beautiful objects managed to grow to such colossal proportions.