BioQuakes

AP Biology class blog for discussing current research in Biology

Author: claireoplast

Thylacine Brain Structure Reveals Predatory Lifestyle

The thylacine, also known as the Tasmanian Tiger, was the largest carnivorous marsupial of modern times. Native to Australia, Tasmania, and New Guinea, the thylacine quickly went extinct at the start of the twentieth century, following an increase of demand for its pelts. The last known thylacine died in 1936, in Beaumaris Zoo in Hobart, Tasmania, and little is known about the species’ natural behavior. New research however, gives humans a better glimpse into brains and programming behind one of Australia’s most fascinating predators.

Dr. Gregory Berns of Emory University and Dr. Ken Ashwell of the University of New South Wales scanned thylacine brains and reconstructed neural connections in an effort to better understand the specific functions of the thylacine brain and behavior. Only four surviving specimens of the brain exist, and their study gained access to two of them.

“One was provided by the Smithsonian Institution, taken from a male Tasmanian tiger after it died at the National Zoological Park in 1905. The other specimen, loaned to the researchers by the Australian Museum in Sydney, came from an animal that died during the 1930s.”, claimed researchers.

They compared the structure of Thylacine brains to those of Tasmanian devils. The researchers found that the thylacine brains had larger caudate zones than the Tasmanian devil brains. This suggests that thylacines devoted more of their brains to complex thinking, particularly action planning and decision making.

These findings match with what we know of the two animals. Tasmanian devils are known to be scavengers while thylacines were hunters. The neural rewiring done by the researchers provides anecdotal evidence that thylacines occupied a more complex predatory brain than their scavenger cousin, the Tasmanian devil.

These findings are fascinating because they give us new information regarding an animal less than 100 years extinct. It’s seems strange that we had never gathered much information about the thylacine prior to its extinction. However, the resurgence in fascination and curiosity about the animal is exciting to see. Hopefully new research and discoveries will be made in the near future, shedding more light on the thylacines life.

 

 

Image result for thylacine

Source Article: http://www.sci-news.com/biology/thylacine-brain-structure-04549.html

 

Gut bacterial and fungal community interactions identified for first time as a factor in Crohn’s disease

Recent studies have found that the interactions between the gut bacteriome and mycobiome are closely related to the development and severity of Crohn’s Disease. Crohn’s disease is an inflammatory bowel disease, that causes inflammation of the lining of your digestive tract. It can lead to abdominal pain, severe diarrhea, fatigue, weight loss and malnutrition.

In the past, the majority of studies have focused on the bacterial microbiota (bacteriome), and little attention has been paid to the fungal lining of the stomach (mycobiome). In a recent study, led by Professor Mahmoud A. Ghannoum from teh Center for Medical Mycology at the Case Western Reserve University in Cleveland, Ohio, has found new bacteria and fungi interactions that may play major roles in the development of Chron’s Disease. In his study, Prof. Ghannoum found an increase in possible pathogenic bacteria and a decrease in beneficial bacteria in CD patients.

Three organisms often found included the S. marcescens, C. tropicalis, and E. coli. The three organisms work together to create a bio film on the inner linings of the stomach. As we’ve learned in class, bacteria are unicellular organisms. They have no nuclear membrane, making them Prokaryotic. The three organisms C. tropicalis, S. marescens and E. coli were highly correlated in individuals with CD and may be key determinants of CD development.

I found this study fascinating because it brings us one step closer to discovering the possible causes of Crohn’s Disease. Approximately 1.6 million Americans suffer from Crohn’s Disease. Finding a cause, would be a huge gain in trying to find a cure. Having a loved one who suffers this disease, it gives my family and I hope for a healthy and pain free future. The questions I’d have, is why do those three specific types of bacteria increase in Crohn’s patients? Or how do they get there in such large numbers?

 

Main link: http://www.gutmicrobiotaforhealth.com/en/gut-bacterial-fungal-community-interactions-identified-first-time-factor-crohns-disease/

 

Secondary sources: http://cid.oxfordjournals.org/content/44/2/256.full

https://www.ncbi.nlm.nih.gov/pubmed/19817674

Insulin Resistance Reversed by Removal of Protein

By removing the protein galectin-3 (Gal3) from the insulin receptor cells, a team of investigators led by University of California School of Medicine researchers were able to reverse diabetic insulin resistance and glucose intolerance in mice with diabetes. This could be the beginnings of a break threw in the cure for type 2 diabetes.

By binding to insulin receptors on cells, Gal3 prevents insulin from attaching to the receptors resulting in cellular insulin resistance. A research team led by Jared Olefsky MD, discovered that by genetically removing Gal3 or using pharmaceutical inhibitors to target it, insulin sensitivity and glucose tolerance could be returned to normal. Olefsky stated, “Our findings suggest that Gal3 inhibition in people could be an effective anti-diabetic approach.”

Gal3 is secreted by microphages (specialized cells that destroy targeted cells).The researchers pinpointed macrophages coming from bone marrow as the source of the Gal3 that causes insulin resistance. The accumulation of macrophages in the liver cells, fat cells, and skeletal muscle cells, leads to chronic inflammation and insulin resistance. The Gal3 released by macrophages causes insulin resistance by binding to insulin receptors on cells, preventing insulin from attaching. The worst part is that Gal3 also acts as a signaling protein, attracting more macrophages to the area, which then produce even more Gal3.

This discovery although untested on humans yet, could be the beginnings of a cure for type 2 diabetes. As a member of a family plagued by Type 2 diabetes, this study can offer hope to us and millions around the world. My main question/ concern, would be is this a one time procedure? Or a recurring treatment?. Either way, this discovery is a huge step for the diabetic community around the world.

 

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Beauty is Pain: and naked mole rats have neither

The naked mole rat is the ugly duckling of the rodent family. These small rodents can live up to 32 years, are virtually resistant to cancer, and have evolved to become immune to certain types of pain. Beneath its wrinkled, fleshy surface, the naked mole rat is the closest animal we have to an indestructible species.

A new study published October 11 in Cell Reports offers some reasons behind the rodent’s abilities. Minor evolutionary changes to the amino acids in their pain receptors make the naked mole rat highly insensitive to pain after birth.”We think evolution has selected for this tweak just subtly enough so that the pain signaling becomes non-functional, but not strong enough that it becomes a danger for the animal,” says lead author Gary R. Lewin, a professor at the Max-Delbruck Center for Molecular Medicine in Berlin, Germany.

Much of this is due to the environment and behaviors present in the mole rats life. Naked mole rats often live in large colonies, with up to 300 members. The constant digging of tunnels and over crowding should leave the mole rat in great discomfort, and highly prone to a condition called thermal hyperalgesia. Humans have the same condition, which we generally call heat sensitivity. Imagine entering a hot bathtub with a bad sun burn. When this happens, it’s because sensory receptors on your skin have been chemically “sensitized” by inflammation or high temperatures. Once those receptors are sensitized, even the smallest amount of heat will cause sensory nerves to send signals to the  brain that register this as painful. Naked mole rats lack this reaction.

Through a series of calculated and carefully designed experiments, Lewid and his team were able to pin point what differentiates naked mole rats from all other rodents- a change in their TrkA receptor. They discovered a switch of just one to three amino acid changes on one section of the naked mole rat TrkA receptor that make it less sensitive.

“Even though the naked mole rat’s version of the TrkA receptor is almost identical to that of a mouse or a rat, it has a very significant effect on the animal’s ability to feel pain,” says Lewin. The naked mole rat is built for efficiency. It’s an animal built to survive the toughest of conditions. Evolution has shut down everything that is not necessary in the naked mole rat, including nerve receptors.

In my opinion, the naked mole rat is pretty cool. It has learned to evolve in order to survive. Maybe this trait is why the this species of rodent in particular outlives all of its fellow rodents by over 25 years. My one question would be, “Is the ability to not feel pain always an advantage? Or can this sometimes lead an animal into dangerous situations?” Whatever the answer, the naked mole rat is an evolutionary success.

 

 

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