The Immortal Cells from Henrietta Lacks

In order to learn and discover more about cells, researchers and even students use laboratory-grown human cells to run tests and experiments. Unfortunately for researchers, keeping a culture/cell line of human cells alive to be used over and over again was proving to be a difficult feat. After a while, the cells would just stop dividing and die off. This was the story until scientists came across Henrietta Lacks' cells. As this article explains, Henrietta Lacks' cells have proven to be  "immortal".

Henrietta Lacks was a black tobacco farmer from southern Virginia who developed cervical cancer at thirty years old. Without Henrietta's knowledge, a doctor from Johns Hopkins took a piece of her tumor and sent it to some scientists. These scientists had been trying to grow tissues in culture for decades but had had no success. They struck success with Henrietta Lacks' cells because for some reason, her cells never died.
Henrietta Lacks' cells, which have been named HeLa cells were the first humans cells to ever be grown in culture. Some of her cells achievements include playing an essential part in developing the polio vaccine and going to space in the first space mission to see what would happen to cells in zero gravity. HeLa cells have also been involved in cloning, in vitro fertilization, and gene mapping.
Over the years, there has been much confusion over the source of HeLa cells. Back in the 1950's, doctors were not too concerned with anonymity in donating samples are they are today. Since the cells are codenamed HeLa cells, when the media would get too close to finding Henrietta Lacks' family, the researcher who had grown the cells gave out the pseudonym Helen Lane, and eventually even Helen Larsen. Henrietta Lacks was not accredited for the HeLa cells until the 1970's.
Henrietta's family did not find out about the HeLa cells until twenty-five years after she died. This came about because a scientists discovered other tissue types, including prostate and breast cells, were HeLa cells. They then found out that HeLa cells could float on dist particles in the air, travel on unwashed hands, and contaminate other cultures. This created a huge controversy, so some scientists decided to track down Henrietta's family to see if they could take her family's DNA to map out Henietta's genes and found out which HeLa cell cultures belonged to Henrietta. This would help them begin to fix the problem of contamination. Since her husband only had a third-grade education he did not understand what a cell was or how scientists still had the cells from his dead wife. The scientists did not know that the Henrietta Lacks' husband and family did not understand what was going on. As a result, her family got sucked into a world of research with the cells basically taking over their lives.
Her daughter Deborah was an infant when Henrietta died. When she found out that part of her mother was still alive, she was desperate to fully understand what that meant. However, Deborah's brothers only became interested once they found out that money was involved. When they found out that their mother's cells helped launch a multi-billion dollar industry, were being sold in vials to people, and that the family got no money from it, they were furious. Most of her Henrietta's family was poverty-stricken. Therefore, her family launched a campaign to try and get what they felt they were financially owed. This campaign somewhat consumed their lives.

Bulky DNA Adducts

As this article explains, Aristolochic acids I and II are two plant toxicants found in the Aristolochiaceae plant family. The acids poison humans by messing with DNA. Metabolic activation of the aristolochic acids leads to the formation of a cyclic N-hydroxylactam product. This product can react with the peripheral amino group of purine bases, thus generating bulky DNA adducts. Therefore, these acids are classified as mutagens and human carcinogens.

Although the AL-dG adducts would with time disappear from the DNA of laboratory animals, AL-dA lesions would still be present in the genomes of the animals. The researchers' data establish a locally perturbed double helical structure that actually accommodated the bulky adduct. The structure did this by displacing the counter residue from the bulky adducts into the major groove and stacking the ALII moiety between flanking bases. The presence of the ALII-dA perturbs the conformation of the 5'-side flanking base pair.However,  all other pairs of the duplex take on their standard conformations. Thermodynamic studies have shown that the lesion slightly decreases the energy of duplex formation in a sequence-dependent manner.

Chapter 9 Helpful Hints!

I found this video to be quite helpful. The video explains the process of G-Protein Coupled Proteins Signal Transduction Reactions. The video takes you step by step through the process. It clearly names, labels, and identifies all of the components of the reaction and explains what is happened at each stage.

When I first clicked on this video I thought it would be a failure attempt at copying a KhanAcademy video. However, once I watched it I realized this was far from a failure. The lecture is easy to follow with many examples and labels. He takes you through the process of signal transduction in terms easy to understand, while still using all of the proper biology terminology. Many of his examples and relations are modern, easy to understand ones that further help you to comprehend the material.

Apoptosis Occurs Because...

Why does apoptosis occur? Apoptosis is defined as programmed cell death, but why would cells program their own death? Also, does apoptosis occur only in higher level organisms or does it occur in organisms like bacteria and fungi as well? Luckily for us, this article answers all of these questions.
Let's attack this question by question. So, why does apoptosis occur? There are several reasons for programmed cell death. To name a few:
1. Some cells are generated in excess and only the ones that become properly functional survive. i.e. Nervous System
2. The mechanism that generates a certain type of cell luckily generates unneeded along with needed cells. Some cells that are needed die with time, but since there were extra unneeded cells produced, the individual is okay. i.e. Immune System
In essence, cells are programmed to die because they are harmful or because it takes less energy to kill them than to maintain them. Programmed cell death occurs to get rid of cells that are not needed, in the way, or potentially dangerous, as Michael Hengartner, the Senior Staff Investigator at Cold Spring Harbor Laboratory, put it.

Now on to another question. Does apoptosis occur amongst unicellular organisms? In a unicellular organism apoptosis could be akin to suicide! Nonetheless, studies have shown processes that scientists consider to be apoptosis in single-celled organisms. The death of the mother cell during sporulation (the process of creating spores) could be considered to be programmed cell death. Some parasites, like trypanosomes change form to escape the immune response from their host. The organisms that fail to change shape just kind of die off.

G-Protein Coupled Receptors and Cardiovascular Therapies

This article explains how G-protein coupled receptors are involved in many types of cardiovascular therapies. Adenosine, a purine nucleoside, activates four G-protein coupled receptors. There four receptors are A1, A2a, A2b, and A3. Activation of myocardial A1 receptors have been shown to inhibit a variety of myocardial pathologies associated with ischemia and reperfusion injury, These pathologies include stunning, arrhythmogenesis, coronary and ventricular dysfunction, acute myocardial infarction, apoptosis, and chronic heart failures. These findings imply several options for new cardiovascular therapies for diseases, like angina pectoris, control of cardiac rhythm, ischemic injury during an acute coronary syndrome, and heart failure.

 The main problem arising involving using full A1 agonists for these problems is the wide range of side effects. This is because of the broad physiologic spectrum of cardiac and extracardiac effects caused by the A1 receptor. This can be overcome by using partial A1 agonists. Partial A1 agonists can be used to trigger only some of the physiological responses of receptor activation. The responses triggered depend on the endogenous adenosine levels and on receptor reserves in different tissues.

Chapter 7 Helpful Hints!

Picture this dearies. It's freshman year and we're about to have a test on cellular respiration. Now cellular respiration was very scary to me since it was complex and what have you. So, in my freshman youth, I searched "cellular respiration song" on Youtube. Alas, the first video I stumbled upon was this video. Now if you sat next to me on the day of the test you might recall me softly humming this. Fast forward two years later and I still remember this song/rap because it was so helpful! The people in the video may be... different, but they nonetheless helped me to remember a lot of the information on cellular respiration. So... enjoy!

Here's another helpful hint! So this song/rap is surprisingly very well done! They go into details that many songs leave out and use many terms that other videos leave out as well. They also go into lipolysis which we briefly touched on, which is when fatty acids are used rather than glucose molecules. So enjoy and brush up on some terms!

Post-Mortum Respiration Leads to Autophagy Gone Wrong?

When a person dies, the person obviously is not able to and therefore, no longer breathing. However, what about the person's cells? Although, the person is no longer respiring, are the person's cells still respiring? Luckily for us, this article answers that question. As of now, it is believed that cell metabolism likely continues for four to ten minutes after a person dies, depending on the temperature around the body. Blood stops circulating, so cellular respiration can only continue for a little while. The oxygen present is used in cellular respiration, and the waste product carbon dioxide is created.

Carbon dioxide becomes carbonic acid, thus lowering the pH of the cell. The acidic environment results in the rupture of intracellular membranes. This rupturing includes the membranes of the lysosomes. Lysosomes contain enzymes which digest all sorts of macromolecules, like proteins, fats, and nucleic acids. Once the lysosome membranes are burst the cell literally begins eating itself from the inside out, resulting in the death of the cell. This process is known as autolysis.

Plants' Homeostatic Reponse to Hypoxia

Plants and animals are aerobes, and therefore require in order to to respire and for energy production. This article explains how the plant response to hypoxia (decline in oxygen availability) is a bit different from the animal response to hypoxia. The decline in oxygen triggers a change in gene transcription and messenger RNA that promote anaerobic metabolism, ergo sustaining substrate-level ATP production. Furthermore, oxygen sensing has not been ascribed to a mechanism of gene regulation in response to oxygen deprivation, like it is in animals. In studying Arabidopsis, researchers showed that the N-end rule pathway of targeted proteolysis acted as a homeostatic sensor of severe low oxygen levels in the plant, through its regulation of key hypoxia-response transcription factors. Researches also found that plants lacking components of the N-end rule pathway expressed core hypoxia-response genes and were more tolerant of hypoxic stress. Hypoxia-associated ethylene response factor group VII transcription factors of Arabidopsis were identified as substrates of this pathway. Enhanced stability of one of the proteins, HRE2, under low oxygen conditions improved hypoxia survival. It also revealed a molecular mechanism for oxygen sensing in plants by the evolutionarily conserved N-end rule pathway.