A Hidden Underclass Created by the Lack of STEM Immigration Reform


    John Oliver


    While international news has been bombarded by reports of Central American children illegally crossing into the US and American news focuses on the crisis of South American laborers flooding across the Mexican border daily, the issue of STEM immigration (Science, Technology, Engineering, Mathematics) often gets swept aside.

    This is an issue that I have a personal vested interest in since I am still dealing with the immigration hurdle myself. Trawling through the internet, I found a variety of opinions, anecdotes and horror stories expressed by those in similar situations as me (e.g. here and here), the most outstanding of which is presented by satirist John Oliver of Last Week Today, formerly of the Daily Show:



    Like John Oliver, I too immigrated from the UK. However unlike him, I was born in mainland China. Because of the archaic rules of USCIS, those who apply for a green card on an over subscribed employment base or family sponsorship base face up to 9 years if born in China and India, up to 20 years if born in Mexico and up to 10 years if born in the Philippines. Of course accomplished scholars with outstanding papers, awards, citations and contributions to the country apply for the green card through the prized "EB1" Extraordinary Ability category. Some are also lucky enough to get their university or company to sponsor their EB1 without needing too many outstanding credentials. Some get married to a citizen (perhaps even illegally!) to obtain the fast-track green card application. However, in the overpopulated world of the academic life sciences, crowded with foreign postdocs such as myself, the chances of acquiring a fast track green card application have dwindled dramatically in recent years, not helped by post-9/11 policies. So many Chinese and Indian scientists are striving for the same high-tier publications in a badly funded system that the likelihood of achieving "National recognition" through a few good papers has sometimes become an unthinkable dream.

    The US government passed a reform bill last year to enable graduates holding F1 visas with STEM degrees to automatically qualify for a green card. This year the Senate attempted to pass another reform bill to add workers employed on H1B visas in STEM fields to this type of faster-paced application. This came as industry leaders, science Nobel Laureates and the White House all acknowledge that skilled immigrants make up the better part of the most competitive companies and the most notable innovators in the US today.



    They also agree that the brain drain of the best foreign graduate students, due to a lack of available employment visas, will be damaging the the US economy. Conservatives may argue that foreign workers, whether skilled or unskilled, tend to take over the jobs traditionally available to Americans, damaging the job market. This a false cry of indignity that is echoed all over the world by anti-immigration parties and right wing groups.


      The Devious Tactic of Delaying Reform


    What has not been said in the immigration debate is that the lack of H1B employment visas and the dearth of visa numbers for green card applicants born in India and China creates a pool of slave labor. The unskilled South Americans who come illegally to the US may pick cherries and mow lawns for a below-average salary. But the skilled foreign scientists who come to the US on H1B visas are also on a very low wage, susceptible to exploitation in a laboratory or behind a desk, with the credits of their work usurped by unscrupulous bosses -I hasten to add that luckily, this has not been my experience! I have seen foreign scientists come to the US and made to work seven days a week with no extra pay and very little result. They are given little hope of finding a job afterwards so are forced to return back to their country after their fellowships ended. This often happens against their will and because they do not dare to protest in light of their visa circumstances.



    Pharmaceutical and biotech jobs, particularly in the life sciences, have traditionally been the go-to career for scientists unable to stay in academia. Such jobs may once have been readily available to US born workers graduating straight out of college. But companies rarely sponsor foreign workers on an H1B visa. Such industrial H1B visas tend to be capped every year. On top of this, perhaps it makes "economic" sense for an American company not to bother with paying a high salary and sponsoring a visa for a foreign migrant who lacks the adequate language and cultural skills to fit the company culture. Or perhaps their branches are being relocated to China and India anyway, which would explain the climate of massive lay-offs. But this is not just a problem endemic to industry.

    Certain benefits of higher education, available to those born in America, such as discounted tuition fees for long-term residents and student loans, are also barred from foreign workers, regardless of how long they have lived in that city. A basic undergraduate course unit at my local community college, which would cost $150 for a resident, would cost me over a thousand dollars right now. Discounts only tend to be available if one can prove extraordinary hardship and the threat of persecution from their home country. In light of the fact that more advanced college degrees in the US are a ticket to upward mobility, the lack of such opportunities for skilled foreign workers underscores another fundamental problem with capping immigration numbers.

    So it is the immigrant class who do the grunt work of manual labor, tough lab work or badly paid technical jobs, while citizens can enjoy the fruits of higher salaries and more choices. Hence the tactic of the government slowing down, rejecting or reversing immigration reform plays to their advantage since there is a market for cheap immigrants to enter the country to do work that natives no longer wish to do. Or maybe this is just a gauntlet set up by legislators to test one's perseverance in attaining an American Dream.

    I say all of this with the utmost respect to my American colleagues and friends who worked hard all their lives but have now become unemployed, underemployed and cannot find a job. Admittedly, life is hard for everyone in the modern day globalized economy. Furthermore, not everyone is fortunate enough to earn a STEM PhD degree and not everyone should aspire just to work in these fields. However, considering the fact that foreign skilled workers have founded 40% of all the Fortune 500 companies in the US and continuously contribute to the US GDP every year, there really needs to be more urgency in immigration reform.



      Neuropathic Pruritus - Our Itchy and Scratchy Show



    As the summer heats up all sorts of bugs and critters emerge from the bushes. When I am out walking or hiking around with others I am more susceptible to being bitten by mosquitoes than anyone else. I often wake up the next day with multiple itchy lumps around my body, which I fight the urge to scratch constantly. My itchiness, or pruritus, is induced by histamine release at the site of the inflamed skin, due to the insect bite and usually subsides in a few days. I am very lucky, because there are many forms of pruritus which are far more severe and they are classified into dermatological, systemic, neurological and psychogenic.

    One of the most baffling is Neurological Pruritus caused by neuronal or glial damage or by endogenous opioids. While some neuropathies manifest as pain, others manifest as itch sensation but no one knows why one sensation is activated over the other. Just as in pain, where responses can lead to peripheral and central sensitization, allodynia (innocuous stimulus causing pain) and hyperalgesia (small stimulus causing heightened pain), the itch response can lead to alloknesia (innocuous touch stimulating itch) and hyperkinesis (light touch or heat causing increased itchiness). In fact the signals for pain and itch are both carried up the nociceptive unmyelinated C-fibers and thinly myelinated A-delta fibers from the skin to the central nervous system. Receptors for pain (nociceptors) and receptors for itch (pruriceptors) are often localized to the same nerve endings, which explains why neuropathic itch is often accompanied by pain. Furthermore, neuropathic pruritus can be activated by at least two distinct pathways, one mediated by histamine release, activated by capsaicin and one which is PAR-mediated, activated by cowhage.

    dermalItch is caused by stimulation of nerve endings in the Dermo-epidermal junction

    In the brain and spinal cord, if a lesion occurs somewhere along primary afferent sensory neurons, either due to injury, tumour growth or aneurysms, this can trigger neuropathic pruritus and manifestation of chronic scratching in patients. In certain neurological disorders like multiple sclerosis, where demyelination occurs, pruritus can also appear in patients. In the peripheral nervous system, ganglionopathies such as postherpetic itch, caused by herpes zoster (shingles) is most commonly known to induce neuropathic pruritus and pain. Small-fibre neuropathies, caused by a variety of other aetiologies is also a common cause of itch.

    Typical presentation of Trigeminal Trophic Itch syndrome caused by postherpetic itch. The patient scratches himself due to damage in the trigeminal nerve.

    This latest review in Nature Reviews Neurology nicely summarizes the list of known causes for neuropathic itch and some current treatments:

    Nat Neurol

    Clinicians often have a hard time distinguishing between neuropathic pruritus and dermatological disorders. According to the review, proper diagnosis should include skin biopsies to measure IENF density, electromyography and tests for sural nerve conduction. Only when the itch is diagnosed as localized or generalized can a set of opioid, acupuncture or neurostimulation treatments be applied.

    It is interesting that so much research has been done on neuropathic pain in the fields of spinal cord injury and certain neurological diseases but so little attention has been paid to itch. There may be room for development here.




      Curing Mitochondrial Diseases and Repudiating this "3-Parent-Baby" Nonsense


    Recently I heard a report on NPR about the new "1 Baby, 3 Parents" treatment. Despite the titillating title suggestive of another social commentary on Polyamory and progressive marital relationships, this was actually a story concerning the public consultation of treating mitochondrial diseases.

    What are Mitochondria??


    Mitochondria are essentially batteries in our cells. They exist to convert metabolites into ATP, generating 90% of energy which power our cells, enabling us to move, think and live everyday. The quirk about mitochondria is that they began in evolution as single celled bacteria which invaded eukaryotic cells 109 years ago to form a symbiotic relationship. This means that they are encoded by a separate set of DNA from nuclear DNA, encoding the bulk of our genetic information. In most people mitochondrial DNA is inherited from the mother. Thus, mitochondrial mutations are carried in the mother's eggs and is a genetic disease.

    What are Mitochondrial Diseases??

    Mitochondrial diseases affect 1 in 250 births and 1 in 10,000 people are sufferers in adulthood. Diseases of mitochondria are caused by mitochondrial DNA mutations which result cell injury and death. Most damage is caused in the brain, heart, liver, skeletal muscles, kidneys, endocrine and respiratory systems, where energy usage is heaviest in the body. The United Mitochondrial Disease Foundation in the US and the Rare Mitochondrial Disease Service in the UK give a good list of diseases which ensue from mitochondrial breakdown. In fact, many neurodegenerative disorders, such as Multiple Sclerosis, which I mentioned previously, may be associated with mitochondrial disease.

    What is the excitement all about??

    A few years ago, a group of scientists in Newcastle University, England, discovered a way to carry out IVF-based nuclear transfer, while preserving host mitochondrial DNA. The technique transfers the nucleus of a fertilized egg (donor zygote) into another egg (recipient zygote) after the host nucleus is removed (enucleation), while preserving the mitochondria from the host. This technology essentially allows the father and mother (the mother being the carrier of the diseased mitochondria genes) to preserve the bulk of their genome in the nucleus, while using another woman's egg containing healthy mitochondria. The new embryo effectively still contains genetic information from the original two parents. Initial experiments have shown that the nuclear transferred-eggs divide normally into blastocytes for up to 8 days, ready for pre-implantation. This could prove to be a vital treatment for people who have a family history of mitochondrial diseases and plan to have children. See diagram:

    Pronuclear Transfer

    They published some interesting reports in Nature here:

    Nature 1

    and here:

    Nature 2


    The fuss in the media!

    This should be a safe technique, which, if trials are successful, can be implemented to rid the world of another dozen intractable diseases. As with all novel innovations, however, people are liable to be concerned with misuse of this technology in designing healthier children, or making "designer babies". A panel in the UK has been set up to review the policies on taking this technology into the clinic. They recruited Doug Turnbull, one of the original scientist on the paper, to advise the panel.

    Understandably, religious and conservative groups are the first to wrangle with this policy. However the media exacerbates the problem by highlighting sensationalist titles of "3-Parent Baby plans". Typical offenders like the Daily Mail and this Christian magazine are exceptionally adept at turning stories of scientific progress into facetious trollop. But occasionally some news outlets (the Guardian) get it right and do a good job of giving a balanced, informative message.





      Multiple Sclerosis and Axon Injury: the new perspective


    Multiple Sclerosis (MS) is a devastating disorder affecting more than two million people worldwide, occuring more commonly in women. It is an autoimmune disorder, which in susceptible individuals, results in the subject's own immune system attacking and damaging the myelin sheath of the nervous system, causing demyelination and neurodegeneration. Symptoms often include fatigue, numbness and tingling of arms and legs (ref. above picture of feet!), walking difficulties, vision problems, cognitive impairments, dizziness, pain and involuntary muscle spasms and paralysis.

    Typical nerve cell (neuron), wrapped in myelin, attacked by the patient's own immune defence (T-cells):

    Patients who suffer from MS often experience a primary phase of inflammation with relapse and remission followed by secondary progressive MS in later years. There is no cure for MS and it is unknown what triggers the initial onset of disease.

    Traditionally, people have speculated that the trigger could be genetic, environmental, exposure to other bacterial or viral infections, or even demographic. However, MRI scans of some patients reveal a new sub-class of MS called normal-appearing white matter (NAWM) in which myelin is NOT damaged and injury correlates with diffuse inflammation in the brain:

    Typical MRI scans of MS patients' brains showing black holes:

    Increasingly it has been found that axon loss can occur early on in the disease, in unmyelinated axons of the grey matter, or in the retinal nerve fibre layer of the optic nerve. This paves the way for a new hypothesis: that MS is primarily a disease of axon injury and neurodegeneration. An article published in Nature Reviews Neurology this year delved into the mechanism of axon injury. These situations are rather similar to damage from a stroke, or to long-term spinal cord injury sufferers. Here is a fancy diagram showing a myriad of ways an axon can be damaged:

    Molecular mechanisms that cause axon damage can essentially include:

    * Inflammation by macrophages and microglia which cross from the blood to the brain

    * Oxidative stress, caused by free radicals, generated by inflammation

    * Mutations in mitochondrial DNA, generating more free radicals and causing loss of ATP (the body's energy molecule)

    * Ion channel dysfunction caused by excess Calcium and Sodium ion influx into the neuron

    * Apoptosis by Wallerian Degeneration (a process where the axon dies back and the neuron eventually dies)


      Pint of Science Philadelphia



    Interested in IPA draft beer and also in brain, body, earth and physics? Come to the Bourbon Blue and Barren Hill pubs in Philadelphia next week.

    Next week (May 19th - 21st) will be the first Pint of Science event in Philadelphia, which aims to bring scientists from the office / lab to the local brewery and give beer-loving enthusiasts the chance to listen to what we really do at work. Since its inception in London, this event has been a tour de force garnering wide spread media attention in the UK and around the world. What with 21 cities and 5 countries participating I think this calls for a new revolution that will rival the Arab Spring, albeit a less violent version.

    I have mentioned this event before here. We have been working hard at assembling and promoting it on social media, in the newspapers and by handing out flyers. If we had more time, we would have reached NPR radio and some TV advertisers. But, the fruits of our labor will soon be ripe for the taking. Here is the schedule of speakers:

    Some amazing speakers include:

    Ted Daeschler, the paleontologist who appeared on the Colbert Report:


    Adam Zolkover, a fermentation expert who has an activist blog and was featured on NPR's The Pulse:

    Andrew Spence, an engineering professor who builds robots to study how animals move:



    Oh, and don't forget to check our social network sites. We have token prizes to give away:

    Facebook: https://www.facebook.com/PintofSciencePhilly

    Twitter: https://twitter.com/PintofSciencePA

    Meetup: http://www.meetup.com/Pint-Of-Science-Philadelphia/?scheduleNow=true




        Tracing Neuronal Circuits 2: The Mesoscale Connectome


      This new article in Nature came out recently and I found it fascinating, since they use a similar technology to us.


      Hongkui Zeng and colleagues have used AAV-EGFP to trace the entire mesoscale architecture of the mouse cortex. Macroscale regions of the brain represent volumes greater than 1 mm cubed. Microscale connectivity represent regions smaller than 1 mm cube, visualized by the electron microscope. Mesoscale connectivity aims to describe large and small regions of connectivity, bridging the differences between the Macro and microscale. This paper is the first instance that anyone has used AAV-EGFP viral tracers to analyze the mesoscale connectome of the adult mouse brain for the Allen Mouse Brain Connectivity Atlas.

      The authors used AAV-2 with a synapsin I promoter (mostly neuron specific). They collected 469 images after injecting various sites that covered the whole brain (I feel sorry for the person who had to do the endless number of injections!?). In total they mapped 295 brain structures to their connections. They promise this is only Phase I of II. In Phase II they will use a Cre dependent AAV vector, presumably to map the secondary order projections.

      Interestingly they use systems computational methods such as graph theory, cluster analysis and network motifs to provide quantitative connectivity data for the vertebrate brain, which hitherto has only been done in C. elegans. Here are some cool images they published:


      3D tractography paths, tracing the topographical projections between the cortex, striatum and thalamus. Two hemispheres of the cortex shown in d. Ipsilateral caudoputamen shown in e. Top-down view of the ipsilateral thalamus shown in f.


      AAVCortical neurons are labeled with AAV-EGFP (Green) and conventional BDA tracer (Red) and DAPI counterstain (Blue). AAV and BDA was injected into the same site at the motor cortex (Yellow, MOp). Confocal imaging shows uptake of the BDA tracer overlaps with the AAV (b, b' and b'').


      corticalCortical projections in the contralateral primary motor cortex (c), ipsilateral primary somatosensory cortex (d), agranular insular area (e) and prirhinal cortex (f) labeled with the same tracers mentioned above.


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Previous Posts

Retiring the Mouse Model Gold Standard

Brexit Britain I weep for you


Seven Years in Visaland

Photo Website

Restimulating the Party

Start Talking Science

A Journey into my Genome

Patent Law IX, The Limits of Biotech Patents

Patent Law IX, The Longest Patent Extension Battle

Patent Law VIII, Invasion of Patent Trolls into Biotech

Patent Law VII, DTC Genomic Testing

Patent Law VI, Supreme Court and Laws of Nature

Patent Law V, The Dark Web

Patent Law IV, Gaming the Hatch-Waxman Act

Patent Law III, The Brave New World of Biosimilars

Patent Law II, The Everlasting Patent

Patent Law I, CRISPR-Cas9

FDA Law Intro

The Big Idea

Accountability for Retractions

Neuroscience Drugs

Locked-in Syndrome

SCI scar Inhibitor




Neuropathic Pruritus

Mitochondrial Disease, 3 parent baby

Multiple Sclerosis and Axon Injury

Pint of Science Philadelphia

The Mesoscale Connectome

Tracing Neuronal Circuits

Pint of Science


The Brain Initiative

Two more online courses done

Fellowship Awarded

One week

Shriners Fellowship

PVA Fellowship

SfN Itinerary

Online Course Certificates

Systems Biology