Showing posts with label #genomics. Show all posts
Showing posts with label #genomics. Show all posts

Friday, April 24, 2026

Fragmentation and Decline of African Elephant Populations

 A genomic investigation of the effects of declining population connectivity in African elephant species.

Figure 1: A depiction of growing numbers of orphaned elephants quenching their thirst and losing major sources of food supply.

    African elephants were separated by habitat several million years ago into two species: Forrest and Savanna. Forrest elephants have higher heterozygosity and population size; however, savanna elephants have higher rates of inbreeding and genetic load. As their habitats have increasingly declined due to human expansion, limited mobility and genetic drift has become a reality for many populations. The savanna elephant is endangered, while the forrest elephant is critically endangered.
    In the first content-wide genomic dataset treating forrest and savanna as distinct species, 232 genomes were studied across 12 different countries in Africa. This study found that these elephants are known for traveling long distances, maintaining high connectivity between species and genetic diversity. In recent years, these elephant populations have become isolated from one another due to human activity, including poaching, expanding infrastructure and declining agriculture to create habitat fragmentation. Smaller, isolated populations are more susceptible to harmful disease and decline from environmental change. As a major African keystone species, elephants shape ecosystems and support entire food webs. By protecting the genetic diversity of these mammalian megaherbivores, entire ecosystems can be protected for cascade and collapse.

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Sunday, April 12, 2026

Chronic Kidney Disease Heightens in West African Populations

 New findings in the genomics of chronic kidney disease

Figure 1: APOL1 kidney disease can only be studied in humans and Old World monkey species to protect against African trypanosomes.

    Among a multitude of severe types of kidney diseases, rates are significantly higher in black individuals. This disparity can be attributed to the two genetic risk variants of the APOL1 gene on human chromosome 22. One risk variant, known as G1, consists of two amino acid substitutions near the APOL1 C terminus. The second risk variant, known as G2, is a deletion of two amino acids near the APOL1 C terminus as well. This mutation has only been found in individuals with recent West African ancestry, and has proved to be beneficial in enhancing immunity against parasitic infections, specifically Human African Trypanosomiasis that causes African Sleeping Sickness.

    This study consisted of more than 8,000 individuals from Nigeria and Ghana, emphasizing the necessity for early screening of CKD, as transplants and dialysis treatments are extremely costly and rare in most regions of West Africa. These genomic differences in these populations pose greater risk of complications, such as hypertension-associated end-stage kidney failure, HIV-associated nephropathy, and other non-diabetic kidney diseases.

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Wednesday, February 13, 2019

Web Meets Genomics

According to Science Daily, a DNA search engine has been made to identify microbes. Researches have combined their knowledge of bacterial genetics and web search algorithms to build a DNA search engine called BIGSI. This search engine could help researchers monitor the spread of antibiotic resistance genes and understand how viruses and bacteria adapt and evolve. The way this works is BIGSI would be able to detect any new microbial genome in the history of microbial DNA. This program is developed with a HUGE memory capacity and simply needs internet to store and search information.

The BIGSI program allows researchers to compare DNA of multiple bacterial species, and by doing so, we can understand how they are related. One of the main focuses of this project was to study the dynamics of antibiotic resistance. Most bacteria and viruses are responsible for many infectious diseases, and over the years, they have been able to evolve and "survive" the antibiotic treatment, thus becoming extremely dangerous to humans.



I believe that anything that is created in order to help us, especially preventing viruses and infections, is for a good cause. This program has been long in demand, many illnesses have taken place and most people have lost lives due to bacterial and viral infections. Being able to compare and analyze microbial DNA can lead us in preventing such outbreaks. For example, the outbreak of food poisoning, where the cause (which was found later) was a Salmonella strain, could have been evaluated earlier with a new and faster system as the BIGSI.

Monday, April 2, 2018

Alcohol Damages Mouse DNA




A metabolite of alcohol known as acetaldehyde, which occurs naturally at low levels, causes double-stranded breaks in the DNA of mouse blood stem cells, according to a study published (January 3) in Nature. Unrepaired breaks can lead to large deletions and chromosome rearrangements, and the mutations are passed on to daughter cells that make up the blood.

Normally, the enzyme aldehyde dehydrogenase 2 (ALDH2) quickly oxidizes acetaldehyde into acetate, which cells use as a source of energy. But many people, including millions in Southeast Asia, carry mutations in the ALDH2 gene that causes the accumulation of acetaldehyde. These people, who are known to have an increased risk of developing esophageal cancer, may also be more susceptible to blood cancers, if the new results hold true in humans: ALDH2­ knockout mice suffered four times as much DNA damage as their wildtype counterparts after alcohol consumption, according to the study.

Research provides very strong evidence that an alcohol metabolite causes DNA damage to the important stem cells that go on to make tissues.

Friday, November 3, 2017

Scientist discover 27 genes that could halt cancer




       Once again, I decided to post about taking another positive step in the right direction to curing cancer. I know that we will eventually have a cure, it is just the journey of finding out more information about our cells in our bodies. The article that I chose was written by Honor Whiteman. It explains the brilliant study done by a few scientists at the Francis Crick Institute in the UK on suppressor genes in the body. 
     Human cells have two different copies of tumor suppressors. The difficulty of dealing with tumors in humans is that its extremely difficult to determine what suppressor copy isn't working. When a tumor forms, it means that both of these copies of suppressors aren't working properly. The scientist created a model that is able to study which suppressor genes are used when a tumor is present. They studied over two thousand tumors over a spectrum of twelve cancers.  The overall result of this study is that they were able to notice 96 gene deletions. What new information that was found was that 43 of these were suppressor genes are 27 were unknown. These new unknown genes will help fight tumors and cancers in humans. What they found will most defiantly help future medicines with suppressing different tumors or at least acknowledging what suppressor isn't working properly. 


Link: https://www.medicalnewstoday.com/articles/319943.php