All posts by Brian LM Cheng

博士学位工资比较(2017-2018) – 更新板






接下来,我们将这笔津贴列为由Pew Research提供的“你在美国中产阶级计算器”中。

Stipend Comparison for PhD programs (2017-2018) – Update

As a follow-on to a popular post in understanding how PhD stipend in each university has progressed, we have again collected stipends from top universities in the US according to USNews.

We were able to extract most of the top 15 universities in their list established this year.

First of all, before looking this deeper, we should keep in mind that the PhD student enrolled in the business sides generally get higher stipend. For instance, A PhD student in the business school at the University of Chicago receives $40000/yr compared with $31500/yr for PhD student in the chemistry/biological science in the same school. The whooping 27% difference in salary doesn’t justify for the difficulties between departments – but we should leave that discussion for another day. This discrepancy is also seen in Harvard University (as shown in orange above).

Next, we ask if we can compare the stipend at each school. To do that, we adjust each stipend to a stipend to live in Chicago according to the cost of living  supplied by the calculator found on This is what we found:

We realize that the average stipend from the list above comes out to be $30061/yr.

Next, we put this stipend level into a “are you in the US middle class calculator” provided by Pew Research.

Honestly, living on a PhD stipend with a full tuition scholarship is really not a bad idea, if you like the fact that you will be submerged in an academic-centric world for the next 5-10 years.

The differences among schools and programs indicate the differences in support for each specialty. The reality is that the business related graduate program is paid higher in general compared with other specialties. Then, it is the sciences, followed by the arts and humanities at the bottom. 

It would be great to see some changes to fix this issue. We feel that graduate students across specialities should not be treated differently. Every students should be provided with equal amount of help, including financial support. 

miRNA takes the center stage of neuropathic pain

A recent publication in Science has touched on the importance of miRNA in regulating major processes in our neuronal system. This paper published by Ernfors group from the Karolinska Institute in Sweden has identified miRNA-183 (miR-183) as an important regulator of neuropathic pain. I found it quite interesting as it highlights the essential, and novel role of miRNA in how we sense pain.

The way how we sense pain can vary depending on our genetic makeup, and during neuropathic pain, mechanical allodynia involves “hypersensitivity of nociceptive neurons and recruitment of touch-activated low-threshold mechanoreceptive LTMR neurons into the nociceptive network”.

Previous research had identified the miRNA-183 cluster is important in regulating pain – over-expression reverse chronic pains, while downregulation causes pain. Emfors group in this paper identified the location of transduction and where miRNA acts on during neuropathy.

In a conditional knockout of miRNA-183 deficient in all neurons, the group found that mice are more susceptible to mechanical pain. This pain is reversible by a marketed drug, called gabapentin (also known as Neurontin), that is commonly used to treat epilepsy, neuropathic pain and hot flashes.

Pt1: Pt2: 

The group then started to tease out the targets of miR-183 cluster. They identified 18 up-regulated and 15 down-regulated genes, when comparing dorsal root ganglia from conditional KO and control mice in RNAseq. mRNA of Cacna2d1 and -2d2 of pain sensitivity by regulating calcium channel are of interest, as they were both increased in the KO mice. They hypothesized that the dysregulation (deletion) of miR183 cluster leads to increase of 2d1 and 2d2, and that lead to neuropathy (in this case, hypersensitivity to mechanical stimuli)

SNI-induced dystonia was found to correlate with higher response to mechanical stimuli when they delete miR-183 cluster specifically in the LTMR neurons, which can be reversed by Gabapentin. This state was also associated with an increased expression of 2d1 and 2d2. This means that these LTMR neurons could produce pain during neuropathy that can be reversed by gabapentin.

Pt 3: Pt 4: 

I guess the big question is how this could be translated into attenuating neuropathic pain in humans. The perception of pain is greatly influenced by our genetic makeup. Identification of specific SNPs in miR-183 cluster that are associated with pain-related disease could be of interest. Using miR-183 to target Cd1 and Cd2 and its targeted genes could be also used as a therapy, however it is unclear how we can specifically target miR-183 on the neurons that matter.

miRNA-based technology and therapeutics still seems to be relatively early. There definitely seems to be great disruptive potential as a potential therapy. But there is certainly concerns regarding understanding its targets and delivery mechanism. Here are the clinical trials ongoing with miRNA: