Buggy Transportation

All the bugs in the metro, tube, subway, from NYC to Asia

By Jesica Levingston Mac leod, PhD

The New York City (NYC) subway is use for more than 5 million passengers per day. Passengers being humans, pets, bacteria, parasites, viruses and other unknown creatures. Consequently infectious diseases, like influenza can be easily transmitted in this transportation method. Other dangerous circumstances are the black carbon and particle matter concentrations, which In Manhattan are considerably higher than in the urban street level. If you have just ridden the subway, I recommend that you check you washed your hands before continue reading…because, literately, this article is about shit!

Last Month a great research team from Cornell published the studies on microorganisms from 466 subway stations where they found 76 known pathogens (aka “bad” bacteria), and, more interestingly, they found a lot of unknown organisms. This means that almost half of all DNA present on the subway’s surfaces matches no known organism. As they could identified some of the microorganisms, they described that these bacteria were originated in some metropolitan citizen food, pet, workplace… you can actually check which kind of bacteria was found in your favorite/closest subway station… just to be sure what to tell to your doctor next time that you have some infection….

During a year and a half, Dr. Mason, the leader of the group, took samples from materials like the metal handrails in order to collect DNA for the big data genetic metropolitan profile project, aka the Pathomap project. From the 15,152 types of life-forms, almost half of the DNA belonged to bacteria—most of them harmless; However, the scientists said the levels of bacteria they detected pose no public-health problem. The most prevalent bacterial species was Pseudomonas stutzeri, with enrichment in lower Manhattan (aka finance species ;)), followed by strains from Enterobacter and Stenotrophomonas. Notably, all of the most consistently abundant viruses (only 0.03%) were bacteriophages, which were detected concomitant with their bacterial hosts.

Other study done in 2013 in Norway, found that the airborne bacterial levels showed rapid temporal variation (up to 270-fold) on some occasions, both consistent and inconsistent with the diurnal profile. Airborne bacterium-containing particles were distributed between different sizes for particles of >1.1 μm, although ∼50% were between 1.1 and 3.3 μm. Anthropogenic activities (mainly human passengers) were the major sources of airborne bacteria and predominantly contributed 1.1- to 3.3-μm bacterium-containing particles. The peaks are at 8 am and 5 pm, following the rush hours.

Other great discovery was that the human allele frequencies in the subway mirrored US Census data. Within the neighborhoods they found African American and Yoruban alleles correlation for a mostly black area in Brooklyn, Hispanic/Amerindian alleles in the Bronx and they observed that Midtown Manhattan showed an increase in British, Tuscan, and European alleles.

In this globalized world, you won’t be surprised that in the London’s Tube a group of journalist and researchers found more than 3 million bacteria. These data suggested that the average train or bus seat could have more than 70 types of bacteria, plus cold and flu viruses. The North-South Victoria line was the only one that passed the hygiene test.

In a study at the Hong Kong subways system, researchers analyzed aerosol samples in order to find the taxonomic diversity of the “under” microbes. Each bacterial community within a line was dependent on architectural characteristics, nearby outdoor micro biomes, and distance to other lines, and were influenced by temperature and relative humidity.

Altogether these results sound really scary, but I hope that the reader won’t react panicking, but just being aware of the bad pathogens around him/her and carry a hand sanitizer/mask/cleaning aerosol/wipes or just wash your hands with soap! Actually, health officials from the FDA, believe washing hands with soap and water is the best method to get rid of germs.

Darwin’s Finches Revisited


By John McLaughlin

In 1859, Charles Darwin published the now famous “On the Origin of Species,” containing the first presentation of his theory of the common origin of all life forms and their diversification by means of natural selection. One aim of this theory was to explain the diversity of traits found in nature as a result of the gradual adaptation of populations to their environments. This point is elegantly summarized in the third chapter:


[quote style=”boxed”]Owing to this struggle for life, any variation, however slight and from whatever cause proceeding, if it be in any degree profitable to an individual of any species, in its infinitely complex relations to other organic beings and to external nature, will tend to the preservation of that individual, and will generally be inherited by its offspring.[/quote]


A large contribution to this theory resulted from his five-year voyage aboard the HMS Beagle, during which he traveled in South and Central America, Africa, and Australia. Darwin collected a huge volume of notes on various plant and animal species, perhaps most famously the finch species inhabiting the Galápagos islands to the west of Ecuador. Although his finch studies were only briefly mentioned in one of his journals, “Darwin’s finches” are now a popular example of microevolution and adaptation for both students and the general public. One striking feature of these finch species is their diversity of beak shape; finches with larger, blunt beaks feed mainly on seeds from the ground while those with longer, thin beaks tend to have a diet of insects or seeds from fruit.


A recent study published in Nature examines the evolution of fifteen finch species that Darwin studied during his time in the Galápagos. Although previous work has helped construct phylogenetic trees based on mitochondrial and microsatellite DNA sequences from these same specimens, this is the first study to perform whole genome sequencing of all fifteen species. In addition to a more accurate phylogeny, these genome sequences allowed for new types of analyses to be performed.


First, the authors assessed the amount of interspecies hybridization that has taken place among the finches in their recent evolutionary history, and found evidence for both recent and more ancient hybridization between finch species on different islands. The authors then looked for specific genomic regions that could be driving the differences in beak morphology among the different finch species. To perform this analysis, they divided closely related finch species on the basis of beak shape, into either “pointed” or “blunt” groups; the genomes from each group were then searched for differentially fixed sequences. On the list of most significant regions uncovered, several included genes known to be involved in mammalian and bird craniofacial development. The top hit, ALX1, is a homeobox gene that also has previously established roles in vertebrate cranial development. Interestingly, almost all of the blunt beaked finches shared a specific ALX1 haplotype (“type B”) which was distinct from that shared by their pointed beak counterparts (“type P”), and vice versa. Based on the distribution of the “P” and “B” haplotypes, the authors estimated that these two groups of finches diverged approximately 900,000 years ago.


By applying genome-sequencing technologies, these labs were able to shed new light on a classic story in biology. Until fairly recently, phylogenetic relationships such as those described in the article could only by inferred on the basis of external morphology. In a Nature News piece commenting on this study, one of the co-authors remarked on what Darwin would think of the results: “We would have to give him a crash course in genetics, but then he would be delighted. The results are entirely consistent with his ideas.”

Scientists, It's Time to Step Up!


By Michael Burel


For years, I have preached the importance of better science communication. I’m not talking about how scientists talk to other scientists. We’re already good at that. We’re trained to discuss what we do with such specificity and precision that only 10 other people on the planet could possibly understand our research. Kudos, us.


I’m talking about communicating science with general audiences, like your long-distance aunt you only see on Thanksgiving. Or your neighbor who’s wondering about potential vaccine dangers. Or even your local representative who needs opinions on funding research in your field. Scientists truly struggle in these arenas, and we must do better.


Scientists’ inability and apathy  to engage with the public wreaks havoc on society. Barely one-third of Americans understand the basics of scientific inquiry, such as knowing the importance of control groups in drug trials. American students fall embarrassingly behind other countries in international assessments of science and math education, jeopardizing the next generation of science leaders. Scientists and the public remain polarized on several key science issues, including the requirement for childhood vaccines and climate change. And when 80% of Americans support mandatory labeling of food that contains DNA – which is basically all food – because they mistake DNA for being dangerous, we have a problem. (As one of my peer’s quipped: “I don’t see anything wrong with this. DNA is an acid, and acid has the potential to melt my face off.”)


None of these points, however, could ever hold a candle to when I recently learned that my mom has breast cancer. I am petrified. I am petrified to see my mom go through complex surgeries. I am petrified to see her go through radiation and toxic chemotherapy. I am petrified to see her lose her breasts, hair, identity, and energy for life. I am petrified of losing my mom.


I am also petrified of the tsunami of information charging her way. My mom is a model local government employee (she’s the Leslie Knope of administrating county-wide elections), but she doesn’t hold any degrees in science. In fact, she took her last science class more than 40 years ago.


So when my mom was put to a firing squad of doctors, I was worried. They fired complex terminology like bullets, where patients can only recoil with confusion at each hit. Hormone receptor status. HER2. Bilateral mastectomy. Cisplatin. Tamoxifen. BRCA1 and 2. Mosacisim. Triple negative.


“Any questions?” a doctor would gently ask.

“Yes…am I going to die?”


In that moment, I realized why scientists must actively communicate to non-experts. We must arm patients with the knowledge to untangle complex jargon, ask insightful questions that link diagnosis with prognosis, and empower them to be proactive and disciplined in their treatment. Patients should be educated on the evolving research of their disease to provide a holistic perspective on what is known and what is not.


“I want all the knowledge about what’s going on inside me. I want to understand everything,” my mom said. “I want to make good choices for myself. If a researcher gave me more information, I could have a fuller conversation with my doctors. Knowledge makes me feel powerful.”


But by current means, scientists remain insulated from the public. When I asked my mom to name all the scientists she knew, she could name only one: me. “I wish it was easier to get to know more scientists,” she confessed. “When I Google, I don’t know who is a researcher and who isn’t. There’s no way I can understand journal articles, so where do I turn?”


As bearers of scientific information, it is scientists’ civic and moral duty to tell the world what we know. If we don’t, we risk the spreading of misinformation, or even worse, no information at all. In turn, the public continues to view scientists as elitists and their work mysterious, expanding the gulf that divides those with science expertise from those without.


Not only has the public paid for our tenure and research, but they also continue to guide the ebb and flow of research trends by electing representatives and engaging in open discourse. By precluding their rightful access to new knowledge, scientists endanger the public’s ability to make informed decisions about their future and, as in the case of my mom, their health.


I call upon every scientist to engage proactively with the public. Open up your world to those not privileged to it. Stimulate wonder and curiosity in young, impressionable minds. Get representatives on your side about funding research for orphan diseases. Instill hope in patients who have nowhere else to turn. Share what you know, because anything less is myopic and selfish.


Let’s get to work.


A Micro Solution to a Macro Problem?


By Danielle Gerhard

Recent estimates by the National Institute for Mental Health (NIMH) have found that approximately 25% of American adults will experience a mental illness within a given year. Individuals living with a serious mental illness are more likely to develop a chronic medical condition and die earlier. In young adults, mental illness results in higher high school drop out rate. A dearth of effective medications leaves many individuals unable to hold a job, causing America a $193 billion loss in earnings per year. These saddening statistics shed light on the need for better drugs to treat mental illness.


Traditionally, treating a mental illness like depression, anxiety or schizophrenia involves a delicate and perpetually changing combination of drugs that target levels of neurotransmitters in the brain. Neurotransmitters are chemicals produced by the brain and used by cells to communicate with one another. Drugs used to treat mental illness either increase or decrease the release, reuptake or degradation of these chemicals from the cell. The current paradigm is that the disease solely results from neurotrasmitter imbalance. Therefore, research has predominantly focused on the specific types of cells that release them. However, neurons make up approximately 50% of all cells in the human brain. The other 50% of brain cells are glial cells and are responsible for maintaining and protecting the neurons in the brain and body.


One type of glial cell, microglia, are specialized macrophage-like immune cells that migrate into the brain during development and reside there throughout life. Microglia are the primary immune cells in the brain and act as first-responders, quickly mounting responses to foreign pathogens and promoting adaptive immune actions. Microglia can adapt to changes in their microenvironment by protracting or retracting their processes to maintain neuronal health, scavenging their surroundings for dead neurons and cellular debris. Moreover, it has been shown that microglia are involved in the induction and maintenance of long-term potentiation, an event that is critical for synaptic plasticity underlying learning and memory. Only in the past decade or so has this cell type begun to surface as a potential mediator in the development and continuation of mental illness. As a result of decades of neuron-focused experiments, the function of microglia have either been misunderstood or over-looked all together. Two recently published experiments contradict our conventional understanding of the etiology of mental illness.


A new study published in the January 29th issue of the scientific journal Nature Communciations by Dr. Jaime Grutzendler’s team at Yale University highlights a novel role for microglia in Alzheimer’s Disease (AD). Late-onset AD is thought to result from the accumulation of the protein β-amyloid (Αβ). This process is referred to as plaque aggregation and results from reduced Aβ plaque clearance. Because microglia with an activated morphology are found wrapped around areas of high Aβ accumulation, it has been hypothesized that they actually contribute to weakened neuronal projections by releasing small neurotoxic proteins, cytokines, that affect cell communication. Aβ can exist as mature and inert fibrillar Aβ but can also revert back to an intermediatary state, protofibrillar Aβ, which is toxic to neurons.


Dr. Grutzendler’s lab set out to to further investigate the role of microglia in Aβ plaque expansion with respect to the different forms of Aβ. Using two-photon imaging and high-resolution confocal microscopy, the team at Yale was able to show that, for the most part, microglia formed tight barriers around Aβ plaques with their processes, but in some instances microglia left plaque “hotspots” exposed. These plaque “hotspots” were associated with greater axonal and neuronal damage.


These findings indicate that microglia generated protective barriers around Aβ plaques that served to protect neurons from the neurotoxic effects of protofibrillar Aβ. Of note, studies using aged mice revealed that microglia were less effective at surrounding plaques leading to increased neuronal damage. Microglia regulation decreases with age thereby rendering neurons more vulnerable to environmental insults. This cell type is therefore a likely key mediator of neuronal death that leads to cognitive decline and emotional distrubances in patients suffering from AD and other neurogegenerative diseases.


Another recently published study highlights a novel role of microglia in addiction, a chronic disease that afflicts many individuals with mental illness, comes from Dr. Linda Watkins, of the University of Colorado, Boulder. The study, published in the February 3rd issue of the scientific journal Molecular Psychiatry, examines the role of microglia in the rewarding and reinforcing effects of cocaine.


It has long been understood that drugs of abuse cause activation of the dopamine (DA) system in the brain, with increased DA release from the ventral tegmental area (VTA) to the nucleus accumbens (NAc), a brain region important for their rewarding effects. Cocaine achieves this effect by blocking dopamine transporters (DATs) on the cell, resulting in increased levels of synaptic DA and sustained neuronal activity. Therefore, efforts have focused on targeting DATs to prevent the rewarding effects of cocaine and ultimately reduce addiction.


In addition to these established dogmas, recent studies have shown that cocaine also activates the brain’s immune system. Microglia express Toll-like receptor 4 (TLR4) and its binding protein MD-2, which are important for reconizing pathogens and activating the release of pro-inflammatory molecules such as interleukin-1β (IL-1β). Using an animal model of addiction in combination with in silico and in vitro techniques, Dr. Watkin’s team found that cocaine activates the TLR4/MD-2 complex on microglia, resulting in an upregulation of IL-1β mRNA in the VTA and increased release of DA in the NAc. Administration of the selective TLR4 antagonist (+)-naloxone blocked the cocaine-induced DA release and the rewarding effects of cocaine administration in the rodent self-administration behavioral models. Overall, the study concludes that TLR4 activation on microglial cells contributes to the rewarding and reinforcing properties of cocaine. Thus, drugs targeting this system could provesuccessful in treating addiction.


Through these studies and similar reports, it is becoming apparent that mental illness is more than a chemical imbalance in the brain and therefore shouldn’t be studied as such. The two studies highlighted in this article show the diverse role of microglia in the development and maintenance of mental illnesses. A more in-depth understanding of how this cell type interacts with already identified neural systems underlying mental disorders could result in the development of better-tailored drug design.