Good morning all,
We recently described human blood in lecture, noting that it is red in color (of course!), and that its color comes from the hemoglobin pigment inside of our red blood cells.
How about a person whose whole blood is blue?
In the news this week is a report about a woman who used excessive amounts of a common over-the-counter analgesic (benzocaine) which rendered her hemoglobin blue in color:
Persons of low blood oxygen levels are considered to be 'cyanotic', and often have a pale or bluish cast to their skin. If their hemoglobin has been poisoned, it can impair oxygen transport/delivery, at worst, to a fatal degree.
In this case, the blue color was not physiologically problematic. This woman's blood was still relatively high in oxygen content, but contained more cyanomethemoglobin (which causes the blue color) than is normal (few percent). Luckily for this woman, her problem was cosmetic only, and the antidote (ironically, doses of methylene blue) was both simple and effective.
Interestingly, blue blood is perfectly normal in crustaceans (such as crabs and lobsters), because they employ hemocyanin (rather than hemoglobin) for oxygen transport. Their blood is of such great medical utility for testing of toxins and contamination that a large (and controversial) industry is devoted to its collection:
And, there is a known genetic disorder than causes cyanosis to run in (a small number of) families, including the famous 'blue Fugates of Kentucky':
So, the next time you hear the term "blue bloods", you might wonder if it is genetic, pharmaceutical, or crustacean in its basis...
Have a great weekend -
Good evening everyone,
At the end of this week we find ourselves in the midst of a discussion of immune function, first with our lecture yesterday on the immune system (Chapter 7), to be followed by our next lecture on infectious disease (Chapter 8), scheduled for next Monday.
Recall that for tomorrow's class (Friday 20 Sept), we will not meet in person. Instead, I'd like you to read/digest a news article on a current and very relevant immune topic, that of environmental exposure to antigens.
For much of the history of our species, human life and society was based around agriculture, including exposure to domesticated animals. In the last hundred years, of course, that has changed for many, as populations became more urban. During this same period, the use of cleansing and sanitizing products in the household has increased dramatically, culminating recently in the explosion of "anti-bacterial" products, such as soaps, wipes, and tissues.
Most immunologists believe that we have taken cleanliness a bit too far. According to the "hygiene hypothesis", natural exposure to antigens keeps the immune system primed for action, and enables it to make robust responses to actual disease agents. In our ultra-clean worlds, however, many (especially the young children of cleaning-obsessed parents) are coming into contact with fewer and fewer natural antigens, and increasingly their immune systems are ill-equipped to respond to them when they do, leading to a rash (no pun intended) of allergies, sensitivities, or, at worst, autoimmune disorders.
This article explores the "hygiene hypothesis" and some of its implications. As you go through it, I'd like you to consider a few key questions:
- what happens to our immune system when we are exposed to naturally-occurring antigens?
- why should exposure to non disease-causing antigens enable us to better respond to more serious antigens?
- do you personally use anti-bacterial products in your household?
- does this article make you want to reconsider their use, in any way?
Our immune system is wonderfully complicated and powerful, but some think that our social behaviors have evolved faster than is good for it. Perhaps a nice walk outdoors, a swim in a lake, or a picnic in the grass is just what we need...
Have a great weekend - see you on Monday.
Good morning all,
As a follow-up to the news article I last sent, here are a couple of updates on this developing story:
Severe illness and unexplained deaths associated with vaping have continued to occur, and, while no definitive cause has been identified, the majority of cases seem to be linked to the inhalation of vaping substances that are coating or irritating the lining of the lungs, preventing proper gas exchange. Vaping materials often have additives, such as flavorings or oils, that are the prime target. A number of persons suffering respiratory distress after vaping seem to have oils lining their lung surface. As one researcher put it, 'The lungs are designed to encounter gases only. Inhalation of other substances is inherently risky'.
I understand that vaping is quite popular, and I worry (a lot) about how dangerous it is. It is trendy and new, but not well regulated, and too recent to have been well studied. I suspect there will be much more news on this topic, and likely soon many more regulations about what can or cannot be included in vaping materials. I hope that you do not vape - but if you choose to do so, please be informed, for your own safety.
Good evening all,
As I mentioned in lecture on Wednesday, we are still on track schedule-wise, and do not have a chapter planned for Friday of this week. Thus, let's not meet in person for class tomorrow. Instead, I'm passing along (below) a link to a recent news article that I would like you to read, about some of the dangers associated with vaping, a topic that is certainly of the latest health issues of concern. As a former smoker, I know first-hand the 'rush' associated with nicotine; as a physiologist, I know too well the dangers associated with inhaled substances. To me, vaping seems to present dangerous levels of both.
I will occasionally pass along science and health news articles of this type during the semester. My purpose in doing so is to help you to become more aware of topics at the interface of biology and society, and also to help you assess how you obtain your science and health news.
Those of us working in science obtain our scientific news, quite often, directly from the original sources: the people conducting the studies and reporting the results. They publish their findings in science journals, or present them at conferences.
Most people do not obtain science news directly, but hear news via secondary sources, such as news releases from scientific organizations, or news stories from the major news outlets. These secondary reports often are then carried by tertiary outlets (smaller/other reporting sources, including news aggregators and media feeds).
Along the way from source to audience, science news is normally distilled (a lot) - much of the detail is excluded or simplified, and the reports often are boiled-down to singular take-home messages, which may (or may not) be good representations of the original work.
When you browse the links that I will forward, or when you access science and health news on your own, I'd encourage you to delve a little bit deeper into them, to read more than just the summaries, and to follow links back to original sources when possible. I'd also encourage you to think a little about the translation of news from source to consumer, and the reputability of the news outlets that you use.
You will not be formally tested on any of the material in the news stories that I will send you, but I do hope that the material in them makes its way into our conversations.
This first link is from the New York Times, which provides one of the best (e.g., best funded and most reliable) secondary sources of science and health news. They do limit access to only a handful of free articles each month, so I will use them sparingly.
Here's wishing you all a safe and enjoyable Labor Day weekend - see you next week.
Good morning all,
As our term comes to a close, I'll use my last news message to send along the latest news from on ongoing story in exercise physiology that raises interesting, and difficult, questions about sex differences in physiology and the regulation of sporting events.
As we have described in class, both males and females have circulating testosterone, with males generally having much higher levels than females, on average. But, like all aspects of physiology, there is a wide range of what constitutes "normal" values, and there is overlap between the ranges of naturally-occurring male and female levels.
The science of testosterone is fairly well-understood in terms of its anabolic effects. Testosterone enables muscle fiber development to a larger size, and facilitates its maintenance at that size. Testosterone supplements have been used (both knowingly and unknowingly) for decades to help athletes build muscle, and its use was the primary factor which led to the formation of the World Anti-Doping Agency (WADA) and the associated regulations restricting the use of chemicals to enhance the physiology and performance of athletes, especially those competing in sanctioned (e.g., large, high-profile, big money) events.
Over the last few years in particular, however, we have gained an understanding that much of what makes us male or female is not always so perfectly discrete, so categorical. For some aspects of our genetics, anatomy, physiology, and performance, male and female traits are most often clearly binary (e.g., one way or the other). But other of our traits, especially some of our physiology, is not so dimorphic or discrete, and circulating testosterone levels fit into this category.
Males and females generally compete only within same-sex sporting events because, for most events, males hold a competitive advantage. This is certainly true for track-and field race events, which place emphases on speed and endurance. This is not to say that female athletes are in any way unimpressive or not elite - they certainly are, and many would leave male competitors 'in the dust'. But, in general, males outperform females in foot races, and testosterone seems to provide at least some of that advantage, through enhanced muscle size and performance.
Recent analyses have shown that the top female athletes in female track events have testosterone levels higher than the average woman. This is perhaps not a surprise, as these elite female athletes carry more muscle than the average woman as well. We must ask - which came first? Did higher testosterone promote more muscle, which led to racing success? Or does intense training lead to muscle development and an altered hormonal profile? Probably some of both.
This situation has reached a peak in recent years over the case of Caster Semenya, an Olympic medalist who hails from South Africa. By all published accounts, Caster is genetically and physically female, but exhibits hyperandrogenism, a state of producing greater than the normal amount of androgens (male hormones). She is the most-accomplished middle-distance female athlete of the last decade, to the point at which protests against her have been raised, and regulations put in place to prevent her from racing unless she takes medications to reduce her androgen levels. She has appealed those decisions, to no avail.
This issue raises many difficult considerations, from the personal (is this athlete being singled-out? Has her privacy been unfairly invaded?), to the social and political (is this another, familiar case of racism in sport?), to the athletic (is Caster really benefiting from her androgen levels?). As such, it seems unlikely to be settled easily, or soon. Nonetheless, it serves as a useful reminder that natural variability is, well, natural - it is an essential part of what allows us to exist as 7 billion different individuals. There are those among us who are short or tall, thick or thin, slow, - or very fast. Can we really regulate or legislate ourselves into categories, for competition, or for other reasons? Most of our physical and physiological traits vary broadly over a continuum, which means that drawing categorical boundaries may be somewhat artificial. In this case, we seem to have a single physical trait, with a well-understood connection to physical performance, that has become exposed in the very high-profile (and big-money) world of competitive sporting.
As we learn more about physiology, we are likely to revisit this issue many times again, and in new ways. How long will it be before we hear "Is it fair for me to compete against someone who has a better genetic profile than I do?". I suspect that, in the coming decades, we will be discussing less the physiological and hormonal aspects of physical and mental performance, but rather the genetic bases for them instead.
I'm signing off for the term now. I hope that these weekly news messages have been useful to you. This is the first semester that I have used them to this extent, and it has been a learning experience for me. In particular,
In the end, though, I remain very optimistic. Science is "mankind's organized quest for knowledge" (Floyd Bloom), and we already know that "knowledge is power" (Francis Bacon). It is science that offers us the best hope to deeper understanding, new therapies and treatments, new cures, and new adventures. We will encounter many speed-bumps along the way, to be sure. I hope that our course has inspired you to be a part of this quest, and to make the best use of the knowledge that you gain while on it.
Have a great weekend, and best of luck with all of your exams next week.
Good morning all,
As we head into warmer weather, thoughts inevitably turn to outdoor activities. With them comes, of course, exposure to sunlight and its radiation. Natural light offers us warmth, pleasurable sensations, and stimulates vitamin D production. As we have been discussing in lab, sunlight also contains dangerous levels of UV radiation.
One of the safety concepts we hear reported related to outdoor activities is the "UV index". This is a scale meant to represent the relative degree of exposure risk posed by harmful UV radiation. The World Health Organization, in partnership with other health agencies, promotes the use of this index as a way to keep the public quickly and easily informed of their exposure risk. The index is fairly easy to interpret: low index numbers, relatively low risk; higher numbers, more risk.
Behind the index is a fair amount of science, in which measured amounts of UV exposure were assessed for their ability to cause cell and tissue damage. Many of the initial studies were done without direct knowledge of what was changing in cells, or what was driving tissue damage. Now, health scientists are able to marry environmental exposure studies to genetic studies, leading to genetic profiles for many of our genes. For example, we now know that the gene responsible for directing production of the melanocortin 1 receptor (gene MC1R) is often mutated by UV radiation; its mutation is one of the leading agents of skin cancer. The normal role of the MC1R gene product is to regulate the production of melanin (eumelanin) in our skin cells, the same melanin which gives us a 'tan' after UV exposure. We all have different levels of melanin production; those of us with lighter skin produce relatively less of it and are at higher risk of UV damage.
Our lab exercise of the past two weeks demonstrated how even short durations of UV exposure can mutate DNA, and also showed how critical DNA monitoring/repair is to continued health. The plate coverings that we used all provided some degree of protection from radiation. While it may be impractical to cover ourselves with tin foil when we venture outside, sunscreen or even thin cloth provided very useful protection. Remember those plates which were empty of yeast the next time you think about spending long hours in the sun - be sure to use sunscreen!
Have a great weekend -
Good morning all,
As you know, I try to send you an article from the science news each week that is relevant to a recent topic we have considered in our class. Some weeks, that requires a little bit of digging, a little reading beyond my usual outlets for science news. This week, however, there is no need to look far, or wide. Our most recent lecture was on immunity, and the science news has been FULL of stories about the immune system, nearly the entire semester.
This week, there are two major news stories related to immune system function. The first of these is just breaking, and will surely be followed by more news to come: the first widespread use of a vaccine against malaria in Africa. We do not hear much about malaria in this country (even though several thousand cases occur in the U.S. every year), but it is a tropical scourge across much of the globe. It is caused by the malarial parasite Plasmodium falciparum, carried by mosquitoes and transferred between human hosts by their bites. It is very infectious - estimates suggest that more than 200,000,000 (that's 200 million) cases occur each year. It's also very deadly, causing >400,000 deaths per year. Children are especially vulnerable. I heard a news report this week that estimated that every 2 minutes, an African child dies of malaria.
As a disease, malaria is very problematic. Its mosquito hosts are very numerous, widespread, difficult to control, and difficult to avoid. The parasite passes directly into the human host circulatory system during a mosquito blood meal, where it takes up residence inside of red blood cells. Remember that disease agents that get inside of our cells are hard to combat - they are at least partially hidden/protected from immune surveillance, and should they be detected and their host cell destroyed, it results in the net loss of functional host cells, potentially even releasing more parasites to infect other cells. Persons suffering from malaria have symptoms ranging from mild (tiredness, chills, aches) to severe (high fevers, blood clots, kidney damage), and aggressive treatment with anti-parasitic drugs (such as Chloroquine) is normally required. Anti-parasitic drugs can also be used prophylactically (e.g., to prevent infection before it happens), but their efficacy is not perfect and varies considerably against the different strains of the malarial parasite. For all of these reasons, an effective vaccine would be a great benefit.
In the news this week is report of the first widespread use of a moderately-effective, inexpensive, anti-malaria vaccine. It was developed over the last 30 years, following promising laboratory studies (the development of a pharmaceutical, from lab bench to use in human populations, can be VERY long). It is suggested to be only ~30% effective in protecting against malaria. But, if 30% of the hundreds of thousands of deaths that occur each year can be prevented, it will be very worthwhile - imagine being able to create a vaccine that prevents 100,000 deaths each year! In addition, much will be learned from this first really large human trial of the vaccine, and the data that will be collected on its efficacy will likely lead to improvements in the vaccine itself.
The other big story related to immunity this week also relates to infectious disease and immunizations, this time for measles. Measles is a very highly infectious disease caused by the measles virus. It causes rashes, aches, and often dangerously-high fevers, and can be fatal to vulnerable subjects. In most developed parts of the world, measles has largely been eradicated, through successful development and use of the measles vaccine, commonly given as one part of the MMR (measles-mumps-rubella) vaccine. Very recently, however, there are severe outbreaks of measles in several locations in this country (including New York City).
These recent outbreaks in the U.S. have been caused by a combination of two factors. The first is a reduced number of parents having their children vaccinated against measles, in large part due to false information about the potential harm caused by vaccines. Over the past decade, several widely reported (but now discredited) stories have circulated about the use of the preservative thimerosol in vaccines, which has led some to believe that the vaccines themselves are more dangerous than the diseases they are designed to prevent. In addition, the vaccine is so effective that measles is rarely reported, so many believe that it is no longer even necessary. Together, these cause lower rates of vaccination in some populations.
The other causative agent is the introduction of the disease from elsewhere, in these cases from travelers who visited areas in the Middle East, picked-up the virus, and brought it back to their U.S. communities. The symptoms of measles may not appear for weeks after exposure, so persons who carry the virus but do not yet realize it can very easily pass it unknowingly to others.
Vaccinations protect individuals if they encounter an agent of disease, because it primes their immune systems (remember those memory cells?) to make rapid and robust responses upon subsequent exposure to an antigen, such as that of the measles virus. Vaccinations also work at a population level, by reducing the likelihood of encountering a disease in the first place. This is the concept of "herd immunity" - if everyone in a population is vaccinated, the chances of encountering someone who could pass on the disease is very low. Measles is extremely infectious (via sneezing/coughing), such that ~95% vaccination rates are necessary for "herd immunity" against measles to be available. In select populations, immunization rates have fallen well below this level.
This combination of factors (reduced immunization rates, highly infectious virus) leads to disease outbreaks. In addition to large outbreaks in New York and Washington state, several college campus in California began quarantining personnel, in an attempt to control measles outbreaks.
Just as our immune systems are wonderfully adapted to protect us from agents of disease, so too are those same agents of disease evolved to evade our immune defenses. It's an evolutionary 'arms race', and, left on its own, would continue that way. Vaccinations give us a terrific advantage against some infectious diseases - but only if those vaccines are safe, available, and accepted. Are they perfect? Of course not - but the scientific community is very much in agreement that they are better than facing the risks without them. If you hear of anyone near you having measles, make sure that you and your family are protected.
Have a great weekend -
Good morning everyone,
Our lecture on Tuesday of this week described the essentials of digestion, and Thursday's topic followed with consideration of metabolism and energy balance as a whole. In the science news this week is a new study on these very topics, with description of a genetic mutation that influences both.
During our digestion lecture, I noted that much of its function is regulated autonomically, by local reflexes mediated in the ENS. That is to say, the digestive tract functions more or less on its own when food is presented to it. By inference then, regulation of food acquisition controls the overall amount of digestion we perform, and the number of calories we have available to use or store.
Regulation of hunger, food-seeking, and feelings of satiety (satisfaction of hunger, or "fullness") occur largely through the hypothalamus, where a variety of chemical signals are known to promote either orexigenic (food-seeking) or anorectic (satiety) states. These include a number of cryptically-named chemicals such as CART, alpha-MSH, agouti-related peptide (AgRP), and melanocortin (MC), each acting at hypothalamic cells bearing specific receptors for them. A great deal of experimental work over the last several decades (mostly in mouse models) has demonstrated that disruption of their signaling (via increased activation of their receptors, or blockade of them) can cause food consumption and body mass to either increase, or decrease.
Abnormally-elevated body mass to the point of obesity has reached critical levels in this country. Depending upon the guidelines one uses, it has been estimated that 30-40% of adults in this country are obese, with another substantial proportion of the population classified as overweight. Extra body mass is a significant health complication, raising one's risk of a number of diseases (including hypertension and diabetes) and complicating treatment and prevention of many others. As such, there is an enormous research effort underway to explore the roots of obesity. We know for certain that the issue is complex - socioeconomic status, willpower, behavior, access to high-quality foods, and sociality influence our food choices, eating habits, and body mass, in ways that are both many and complicated. Increasingly, there is growing appreciation of genetic components to obesity as well.
Modern genetic assessments of health have benefited by technological advances that allow sequencing of individual genomes, resulting in large databases of genetic information. When these are paired with health profiles and lifestyle data, they make possible genome-wide association studies (GWAS). GWAS represent a powerful way to take two very large sets of data (gene sequences and health/lifestyle data) and see how/where they intersect. In contrast to the twin study I described to you in my science news email last week, GWAS are useful only when based upon thousands (usually, hundreds of thousands) of individuals. These are not experimental methods, so they cannot provide definitive proof of anything, but they can reveal interesting "associations" - places where genetics and health vary in consistent ways.
This new study describes a GWAS that sought genetic bases for obesity. In a very large sample of human subjects (500,000 individuals), the researchers looked for consistent genetic mutations in people who were, or were not, obese. They found evidence for specific genetic variation in the MC4R gene (melanocortin receptor 4) that was associated with obesity: persons whose MCR4 gene was mutated (causing reduced function) were much more likely to be obese that those who carried the 'normal' version of the gene. To some extent, this finding was not new - this effect of MCR4 mutation had been described previously, in smaller studies. Here, though, the researchers also found evidence that if mutations in the gene(s) that regulate MCR4 cause it to be 'turned on' all of the time (instead of occasionally, such as after eating), it causes chronic satiety, or "fullness". Persons with this form of mutation are much less likely to be obese, so the researchers interpret this alteration of MCR4 function as protective, and preventive of obesity.
Thus, we may have a single gene, which if mutated in one fashion can contribute to obesity, and if dis-regulated in another way can protect against it. A second study described in this same article uses similar data to create a genetic risk assessment for obesity, with the hope of reducing its prevalence, potentially by intervening before it reaches criticality.
The genetic associations described in this study are not enormous, just a few percent (perhaps 6%). Still, they represent the largest known genetic association for obesity, and that in and of itself is a very worthwhile finding. Many persons who are obese suffer from anxiety, depression, and feelings of low self-worth, thinking (and too-often being told) that they are 'fat', or overweight, because of their behavior and lack of willpower. What if the problem lies in their genes, and not in their self-control? We all know how difficult it is to resist food when we are hungry - what if that feeling never goes away?
Like most science, these studies raise more questions than they answer. Obesity and weight control are such significant problems, though, that their investigation is crucial to improved public health. Here's to more studies and more information on these topics - they are likely to benefit us at a variety of levels: individually, via our loved ones, or as part of society as a whole.
Have a great weekend -
Good morning everyone,
As we enter the last quarter of out term, we soon will be considering the remaining chapters in our text, on topics including digestion, immunity, metabolism, and reproduction. These are relatively 'integrated' phenomena - complex and intertwined with other of our physiological systems and processes.
In the science news this week is a report that is similarly integrated, on simultaneously both a larger scale (the entire body) and a smaller one (examination of just one person, relative to one other).
Nearly all quality research in physiology (like that of other fields) relies on large sample sizes - studies of hundreds, thousands, or even millions of individuals. The larger the sample, often the greater the statistical power of the comparisons, the ability to detect tiny effects. Does this drug lower blood pressure? How does a vegan diet influence sleep habits? What are the genetic components of immunity? Studies like these would never evaluate one or two subjects, because the ability to generalize the results would be very low. And, studies employing few subjects would be very unlikely to be funded or pursued, for exactly that reason.
But, NASA's study of astronaut Scott Kelly (and comparison to his Earth-bound twin Mark) is quite unique, in many ways: how many of us will ever spend (nearly) a year in space? So, far, perhaps just a handful of people. How many of these individuals have an identical twin? Just one.
Scott and Mark were subjected to a battery of tests before, during, and after Scott's 340 day long space aboard the International Space Station. How does a life in space influence the body? Well, in many ways, as it turns out. Why do we care? Because, as a society, we continue to push the boundaries of space travel, and long journeys in space (to Mars, or other places) are surely on the horizon. What will happen during those trips? Scott and Mark Kelly offer a useful, and unique window into this problem. Because they are genetically identical, in theory, any differences between them should be due to their environments. If they were carefully evaluated before, and then after, Scott's year in space, it should allow us to see what space travel does to the body, by comparing Scott and Mark.
If Scott Kelly is a useful model, life in space will be very challenging, physiologically. Among the largest changes noted upon his return to Earth were cognitive deficits, colonization of his body by different kinds and numbers of bacteria, indicators of high stress levels (no surprise), many genetic mutations, and, surprisingly, longer telomeres on his chromosomes. This last finding was unexpected - telomere length is a sign of cell age, and long telomeres are normally interpreted as a sign of youth. Does space travel reverse aging? Probably not! It's more likely that the rigors of space life (especially the radiation exposure) triggered lots of repair and replacement of damaged cells, and newly created cells may have higher levels of telomere maintenance.
In many ways, Mr. Kelly has offered himself as a 'guinea pig' for these studies - even now, back on Earth for years, many of his symptoms and genetic mutations remain. Was it worth it? His answer is an unequivocal 'yes'. Like other astronauts before and after him, his experiences were literally other-worldly. Our technological advances toward space may be outpacing our physiological ones, however. If Mr. Kelly's response is typical of what will happen to the human body in space, we have much to learn, and much work to do, before long-term stays in space will become feasible.
Not to say that all of the news is negative: he took some amazing photos while he was there:
Have a great weekend -
Good morning all,
In our last two lectures of this third unit of the course, we are considering renal function and the often overlooked role of the kidneys in our health and well-being. During lecture on Thursday, I mentioned several facts related to kidney disease and failure that some recent science news can inform.
We discussed conditions such as diabetes and hypertension that can induce kidney damage and failure, and the third items on that list was genetic bases for kidney ailments. One of the reasons that we did not elaborate on the topic is that the specific genetic causes of kidney disease (like that of so many other of our diseases) is very nebulous - there are many genes involved, often with very weak effects, and their interactions with each other and with environmental influences are poorly understood. In these situations, patients often recognize that they are part of a family history of disease (suggesting its genetic basis), but typically the genes involved are not identified, or their function is not characterized.
Recently, several research teams have made progress on this issue. Using exome sequencing (a DNA sequencing method that focuses only upon the protein-coding regions of our DNA), researchers recently have described with greater detail the number of different genes involved in a small sample of patients with chronic kidney disease. They identify over 60 different genes, some with identified roles as membrane transporters or regulators of gene expression. Most of these were associated with a tiny number of disease cases.
As is often the case, studies like this are useful if only because they reveal how much we have yet to learn, and offer a potential method forward. It's a very long (and expensive) pathway from gene identification, to functional investigation, to testing of therapeutics, to useful treatments, and most avenues of exploration do not yield breakthroughs. But, we now know more than we did, and there is great interest in finding ways to abate kidney disease. There are still a great number of people awaiting kidney transplants, and many die while they wait. Inequities of access to donated organs may be part of the problem. Perhaps we should pay people for organ donation - or would that be more problematic than useful?
Have a great weekend -