Miscarriages Among Flight Attendants

Flight attendants are individuals that assist you during long hours of air travel. They can help in maintaining a personal level of comfortability and safety during a long and tiring flight. Though typically not regarded as a dangerous profession, flight attendants are exposed to many occupational hazards that most have not considered before. These hazards include circadian rhythm disruptions, cosmic radiation exposure and secondhand smoke exposure. Since the 1990's smoking on commercial airliners has been banned due to the high negative health impacts associated with second hand smoke exposure.

                Flight attendants that worked on aircrafts before this ban experienced higher levels of breast cancer and melanoma. In a recent study, researchers discovered a link associated with the flight attendants and miscarriages. A total of 145 flight attendants exposed to secondhand smoke before the 1990’s were found to have a 26% miscarriage rate. This was compared to 17.1% that was reported by the national report from the CDC.

                Overall, it was determined that the flight attendants did in fact have a higher incidence of miscarriage, but it was not related to secondhand smoke exposure. This lead to the thought that the other occupational hazards played a significant role in their increased miscarriage rate. The disruption of the circadian rhythm and radiation exposure are thought to be related to the reproductive health of individuals. Though further investigation is needed, a question that this study invokes would be that should a higher degree of caution be taken towards pregnant flight attendants? This question is relevant when considering the impact of long flight hours and the presence of teratogens during embryological development.

                If considered properly, a future concern would need to be emphasized regarding the specific precautions that would need to be taken with pregnant flight attendants. The goal would be to decrease the time spent in the sky to prevent the possibility of a miscarriage form occurring.

http://www.amjmed.com/article/S0002-9343(17)30611-3/fulltext

Macrophages And Their Role In Heartbeat (In Mice)

Macrophages typically protect the body against invading pathogens, but a new study published in April of this year, shows their role in helping to keep the heart beating. It has been known for a couple years that macrophages live in healthy heart tissue but their role was not known, until now.
Cardiomyocytes, the heart muscle cells, are responsible for contracting in response to electrical signals, pumping blood through the heart. It is thought that macrophages squeeze in between the cardiomyocytes and help them receive the signals and stay on beat. A cell biologist at Harvard Medical School performed an experiment to test their role. He genetically engineered a mouse to not have macrophages and then performed a cardiac MRI. What he found to be interesting was that the heartbeat was too slow and too irregular to even perform the scan. Isolating an individual heart macrophage and testing it for electrical activity did not lead to any answers either. It wasn't until the macrophage was coupled with a cardiomyocyte that researchers saw what they were looking for. When they were coupled, the two cells began communicating electrically.
When in their resting state, cardiomyocytes have more positive ions outside the cell than in. When the cardiomyocyte receives an electrical signal from a neighboring cell, positive ions rush in causing a depolarization and the ability for this cell to contract and send the signal on to the next cardiomyocyte. Previously, it was thought that cardiomyocytes could conduct these electrical signals on their own, but now it is being demonstrated that this might not be the case. Macrophages link to cardiomyocytes by a protein which allows the macrophages to transfer positive charges making it easier for the heart cells to depolarize.
The next step is to determine if macrophages play the same role in humans.

References:
Eaton, Elizabeth. “Immune Cells Play Surprising Role in Steady Heartbeat.” Science News, 16 May 2017, www.sciencenews.org/article/immune-cells-play-surprising-role-steady-heartbeat.

ECMO Ethics: The Cardiologist's Conundrum

Extracorporeal membrane oxygenation (ECMO), is a relatively novel form of bypass treatment, primarily seen in Cardiac Intensive Care Units (CICU) for post-operative patients or the like.  Unfortunately, there are some severe side-effects that are associated with ECMO, which intrinsically sow ethical dilemmas into the already delicate fabric of treatment and care of CICU patients.  

Here's an example of the physiological breakdown of ECMO:  A baby is born prematurely.  As a result, their diaphragm did not have enough time to fully develop in time to breathe on their own.  Left untreated, this will lead to system failure, by lack of oxygen perfusion in the body, suffocating the newborn.  So what are the treatment options?  Most likely, some sort of synthetic diaphragm will be surgically placed on the newborn, and they'll grow up and be healthy.  Great!  Not so much.  Baby still needs to perfuse their little body with oxygen during the surgery and during recovery.   

Blood is drawn from a main vein the baby, typically the internal jugular vein.  The blood is fed through a tube into a rotating drum.  The RPM's on the drum create a negative pressure, sucking the blood out of the jugular.  In the drum, there are hundreds of specialized tubes that will act as artificial alveoli.  The blood is oxygenated in the drum and returned through another tube leading to a main artery, typically the common carotid artery.  

So what's the big problem?  Well, it seems that in many cases, being put on ECMO causes hemolysis, or bursting of the red blood cells (RBC).  The RBC's contain hemoglobin, the protein structure that carries the oxygen.  It turns out that hemoglobin circulating, free from the RBC is toxic in the body (Plasma-Free Hemoglobin), and causes a myriad of issues, especially in the kidney.  This leads to having to place patients on forms of dialysis, or more severely, mortality (Kim et al., 2018).  

If you’re the cardiologist, what do you do?  If you place the child on ECMO, there is a solid probability they’ll develop kidney failure, be placed on dialysis, and may die.  If you don’t do anything, they’ll die. 

What ought to be done?  No ECMO = Certain Death, ECMO = Possibility of Survival.  Previous literature has stated that the RPM values or the degree of negative pressure are what is causing the hemolysis.  Unfortunately, that does not seem to be the whole story.  A research team at Children’s Hospital Colorado is currently looking at these causes, and so far, it appears that the issues are much more complicated, and more research needs to be done.

References
Kim, JS, Hyslop, R, Powers, PE, Stanfield, N, Deakyne, S, Ellis, CW, Gist, KM. (In-Press/2018).  Evaluating the outcomes and risk factors related to hemolysis during extracorporeal membrane oxygenation (ECMO) support with a centrifugal pump. Journal of the American College of Cardiology.

Home Hemodyalysis: The Unknown Option

            Kidneys are very important, relatively easily damaged, and don’t regenerate. Chronic Kidney Disease (CKD) can develop a variety of ways, and is a present and growing public health concern in the United States. As we’ve not only begun developing CKD more frequently, but also living longer, end-stage renal disease (ESRD) has begun to be more prevalent as well. The treatment options for ESRD are pretty limited: Dialysis or a kidney replacement. Kidney replacements themselves are complicated, so I’ll leave that discussion for another blog. Dialysis, technically called Hemodyalysis, is the far more common option of the two, but it’s not preferred.

            Hemodialysis (HD) treatment relies on an external machine to do the work of individuals’ kidneys. HD machines filter patients’ blood (supplied via IV) over ~four hours, and must be done ~three times a week. As you can imagine, this puts a huge burden on patients in time and lifestyle loss.
            Enter Home Hemodyalysis (HHD). This treatment is completed in patients’ homes, alleviating many of the burdens of HD centers. There are no lines or scheduling, and treatment can even be done at night. Research has shown a positive correlation between HHD (especially nighttime HHD) and a decrease in hypertension, left ventricular mass, and patient mortality rates, as well as an increase in overall patient health scores. Despite all of these benefits, HHD is by less than 10% of dialysis patients.

            HHD sounds amazing, so why isn’t it used more frequently? My first assumption is that Medicare must not cover it, but that’s very incorrect. Medicare is actually trying to increase HHD use to 25%, but is having little success. HHD is actually cheaper than in-center HD, which Medicare loves, but providers may not. Simply put, physicians are not reimbursed as much when patients use HHD, so many don’t discuss it. As one paper aptly pointed out, “It is unclear how the regulatory body expects the patient to advocate for themselves if they do not know whether the HHD option exists.” Now, to be fair, HHD is also a little more expensive upfront for patients. Home plumbing and electrical modifications must be done, but these costs would likely be offset by improved lifestyle and time to work. I rarely think it’s appropriate for patients request specific treatment from providers, but in this case, physicians are breaking ethical principles by not informing patients about HHD.

Sources

Dialysis. (2017, June 14). Retrieved December 01, 2017, from https://www.kidney.org/atoz/content/dialysisinfo 

Hajj JJ, Laudanski K. Home Hemodialysis (HHD) Treatment as Effective yet Underutilized            Treatment Modality in the United States. Healthcare (Basel). 2017 Nov 28;5(4). pii: E90. doi: 10.3390/healthcare5040090. Review. PubMed PMID: 29182543.

A cure to "one of the most complex diseases ever described"

        Multiple Sclerosis (MS) is a very complicated disease as it effects both the nervous system and immune system. Evidence shows that a possible cause of MS is the corrosion of the immune system which will break down the nervous system. The incorrect behavior of the T-cell in our immune system can be the first step leading to MS. The T-cell enters the brain due to a disruption in the blood-brain barrier and after the T-cell has entered, it recognizes the myelin as foreign and attacks it. This violent attack triggers inflammation and other immune cells to further break down the blood-brain barrier which effects the communication between neurons. This lack of communication between the neurons then results in the break down of the nervous system in the body.
        Doctors have struggled over possible cures for this disease and have found relatively nothing, besides dietary supplements which can help strengthen an individuals' immune system.  However, there has been a break-through drug called Ocrelizumab. This drug is still in clinical trials and is currently in several different phase 2 and 3 trials.
        The plan behind Ocrelizumab is to target B-cells of the immune system. In theory, this drug will attack the disease-ridden immune cells in order to stop MS. This drug specifically attacks the protein CD20 on the B-cell, inhibiting the cell. Inhibiting the B-cell will stop or slow the inflammation happening around the brain. By discontinuing the function of the protein on the B-cell, the cell will self destruct, inflammation will decrease, and there should be better communication between neurons.
        In the current trials, the results have shown that this drug will help reduce lesions and relapses in about 70% of its patients. The trials surrounding this drug are currently for individuals who have shown symptoms of Relapse Remitting MS.      

Works Cited:

Ocrelizumab. (2017). MultipleSclerosis.net. Retrieved from:    
        https://multiplesclerosis.net/research/ocrelizumab/
Yeager, A. (2017). Scientists are seeking new strategies to fight multiple sclerosis. Science News.  
        Retrieved from: https://www.sciencenews.org/article/scientists-are-seeking-new-strategies-fight-
        multiple-sclerosis

Is it possible to regenerate cardiac muscle after a heart attack?

            When someone has a myocardial infarction, commonly known as a heart attack, there is typically associated cardiac muscle damage that occurs in response to it.  The damage to the cardiac muscle is specifically to the heart muscle cells, cardiomyocytes, which are the cells that help contribute to the pumping and contraction function of the heart. With the loss of cardiomyocytes, it causes for the heart to be unable to pump as much blood per beat, and can be causative for increased rate of heart disease and mortality associated with it.

            Cardiomyocytes are cells that are known to be unable to regenerate, but the reasoning behind this is unsure. With this being the case, Edward Morrisey, Professor of Medicine and Scientific Director of the Penn Institute of Regenerative medicine in Penn Medicine and his team set out to target the cardiomyocyte proliferation pathway to help repair damaged cardiac cells.

            The team of doctors, researchers, and engineers set out to develop a gel using microRNA’s that target the cardiomyocytes specifically, and prevent their “stop” signals from firing, allowing for continued cell proliferation. The gel is injected and is short-lived with only lasting in the bloodstream for about eight hours. The gel has two characteristics that are ideally used to help to directly inject it to the tissue where needed and prevent proliferation of cells in spots where it is not necessary. These characteristics are that the gel is shear thinning, meaning it breaks under mechanical stress and is able to be administered with a syringe, as well as self-healing so when the stress is removed, the bonds in the gel reform and stay intact with heart muscle.

            The gel was tested in three populations of mice under different conditions but all ultimately showing this gel could be promising for promoting repair of cardiac muscle after a heart attack. The first population of mice was normal, healthy mice that showed increased proliferation of cardiac cells identified with the use of biomarkers. The second group was the “confetti” mice, which were transgenic mice expressing four different fluorescent proteins in four different colors. These mice had heart attacks induced, and afterwards saw that there was proliferation and “clumps” of different fluorescent proteins that were in response to the microRNA-gel. The third population of mice had heart attacks induced as well and were tested to see clinical relevance of the treatment. These mice in comparison to the controls showed improved recovery including a higher ejection fraction, or the amount of blood pumped out of the heart with each beat.

Though this gel has only been tested in mice, the research is looking to be able to apply it to human cardiac cells in vitro next. If this gel continues to show promise, it could ultimately lead to a reduction in numbers of those affected by cardiac disease and the damage that comes from experiencing a heart attack.

Sources:

University of Pennsylvania. (2017, November 29). Injectable gel helps heart muscle

regenerate after heart attack. ScienceDaily. Retrieved December 1, 2017 from

www.sciencedaily.com/releases/2017/11/171129131346.htm

Flu season is here but will the vaccine work this year?

          With flu season among us, research of the influenza impact in the southern hemisphere is emerging and preparing physicians for a possibly severe season. Based on reports from the Australian Government Department of Health they had 215,280 influenza cases by mid- October 2017 in comparison to 59,022 cases just six years earlier. The strain of influenza that was observed was Influenza A (H3N2), with the vaccine only being 10% effective. Though the vaccine for the northern hemisphere, specifically the United States, is not necessarily identical, it is of similar composition prompting worry for a very low effectiveness of this year’s influenza vaccine. With a low effectiveness of the vaccine it leaves the young, the old, and those with preexisting conditions more vulnerable for developing this disease and have severe outcomes.

            But what makes it so these vaccines aren’t as effective from one year to the next? As explained by Catherine Paules, M.D. and her team, vaccines are strain specific and from year to year the vaccines require changes six to nine months prior to administration. This means that the composition of the vaccine is developed based on research from global virus surveillance data from the five to eight months beforehand, and not necessarily up to date when the vaccine is created. Influenza viruses are antigenic, and able to adapt and bind to a product of the immune system inhibiting their action, making it hard to create a completely effective vaccine against the disease.

            Catherine Paules and team also presents the information of how not all vaccines are made the same way, in means of the sources of the substrates they are produced from. In the United States, most influenza vaccines are propagated in eggs, which have properties of effecting proteins within the vaccine virus and thus making it less effective. There are other ways to produce the viruses used for in vaccines including in cell culture or by expressing specific viral using recombinant DNA technologies. Research done by a study on the 2016-2017-influenza vaccine that was developed in eggs showed to be less effective in regards to possible mutations in the virus caused by the egg. With this year’s influenza vaccine also being developed in eggs, it is proposed that based on the research from the Southern hemisphere flu season that the United States will experience low effectiveness of the vaccine for Influenza A. It is proposed that in the years to come, for further research to be done on the development of the vaccines and that to make a “universal” vaccine that can handle the antigenic changes of the viruses and even the other strains that are observed season to season.

Citations:

Paules, C., Sullivan, S., Subbarao, K., Fauci, A. (November 29,2017). Chasing Seasonal

Influenza- The Need for a Universal Influenza Vaccine. Retrieved from

http://www.nejm.org/doi/10.1056/NEJMp1714916