Slogging through another election cycle, you are probably deluged with dozens of political ads every day with candidates touting what they will vaguely do for your vote, and often, talking about how much their opponents suck. Don’t you wish they would have more concrete plans, or at least promise to delegate to true experts who want a better quality of life for the citizenry? As you determine which option to go with at the ballot box, perhaps it is time to consider what their position is on important science policy.

Throughout graduate school and even now, I’ve relied on Wikipedia as a valuable resource for quick information. My mentors and teachers have cautioned me against actually citing Wikipedia articles, but often these articles will show up as top searches on Google, and their listed references lead to published scientific articles so I could always go back to the original source and see the data and conclusions for myself. The fact that Wikipedia is free and freely edited makes it prone to fictionalization, which reminds us of the importance of corroborating whatever we read with third-party sources and our own experiences.

The term apoptosis was first used in 1972 to describe a morphologically distinct form of cell death. Since those early experiments and observations, apoptosis has become one of the focal points for biological research, with myriad laboratories and research groups continuing to work to further elucidate the components and pathways that drive this programmed cell death. As a fundamental biological pathway, apoptosis has benefits and adverse effects for the host organism. For example, many therapeutic strategies involve the activation of apoptosis to kill cancer cells, while other treatments seek to prevent apoptosis to preserve precious cells in key tissues. 

As human beings with trillions of cells, each of which has their associated millions of copies of myriad proteins and other biological molecules, it’s something of a miracle that enough of the molecules bump together at the right times to keep us alive and functional. In addition to our own cells, we also coexist with microscopic neighbors, including various beneficial bacteria, while fending off pathogens like disease-causing bacteria, viruses, protozoans, and fungi. We often consider the bacteria and viruses in most human diseases, which invoke our immune systems to fight them to keep us healthy, but it also makes sense that the fungi can affect us as well, a topic in cancer research that is gaining attention.

Many of you are well on your way through graduate school, itching to earn that precious PhD, while some are just starting out, getting ready to take your first midterms while preparing to choose your first research rotations. Regardless of where you are in your career, or even if you've already earned that doctorate and are on your way to a postdoc and beyond, ABclonal's blog series has put together some articles that can help you get through the day. Whether it is experimental troubleshooting or just trying to get along with your lab mates and PhD supervisor, here is a collection of previous blogs that should be of use to you. 

Reaching the golden years doesn’t always feel so golden. As we age, disease, injury, and other stress factors from the environment will damage our bodies' cells. Most cells may be able to repair that damage, while our immune system usually clears those damaged cells through a process called apoptosis.^[1] However, if cellular repair and clearance is not effective, the residual damaged cells will further weaken the immune system and deteriorate other biological processes. Is there a possibility that we can avoid this cellular damage and improve the health of older people? A cellular state known as senescence might hold the key to this question.^{[1, 2]} During senescence, the damaged cells irreversibly stop dividing and resist being removed. ^[3] Researchers have shown that determining senescence biomarkers could lead to new therapies for the inflammatory disease caused by senescence in older people.^[4]