A new method inspired by kid’s pop-up books for making 3D artificial tissue was reported by Cory Nealon, University of Buffalo (NY) for Phys.org, 15 October 2021.
University at Buffalo researchers have developed a new process for creating three-dimensional artificial tissue, an advancement that could improve experimental drug testing, the quality of artificial organs, and more. Described in Advanced Science, the method is based upon compressive buckling—the structural engineering principle that explains why figures project outward from the pages of children’s pop-up books.
“When you turn to a new page, you create force. This force pulls on the feet of the figure, which forces the folds to open and the figure to pop out,” says the study’s co-corresponding author Ruogang Zhao, Ph.D., associate professor of biomedical engineering. “With this study, we have shown the same principle can be applied to artificially engineered tissue.”
To showcase the method’s utility for tissue engineering, the team created an osteon-like structure. Osteon is the basic building unit of bone tissue and is characterized by osteocytes sparsely distributed in a mineral bone scaffold. Each osteocyte rests in a small cavity, known as lacunae, and different osteocytes are connected through canaliculi, which are small channels in the bone scaffold.
The results are important, Zhao says, because most tissue engineers rely on two-dimensional tissue fabrication methods to create very thin tissues that do not represent the volume of the human tissue. The planar nature of these tissue models limits their application in disease modeling and drug testing, he says. The compressive buckling method can be used to rapidly transform a two-dimensional tissue to a three-dimensional tissue with substantial thickness, thus allowing researchers to create more realistic tissue and opening new possibilities in tissue engineering and regenerative medicine. It also has the potential to outperform other method of 3D tissue engineering, such as 3D bioprinting, in terms of the fabrication speed and spatial resolution, Zhao says.
Several beta cell receptors could explain link between COVID-19, new-onset diabetes was published by Healio.com/Endocrinology, 15 October 2021.
SARS-CoV-2 may use ACE2 or other enzymes as a receptor to infect beta cells, providing a possible explanation behind new-onset diabetes occurring in people with COVID-19. “COVID-19 results in a significant increase in new-onset diabetes,” Irl Hirsch, MD, an endocrinologist and professor of medicine at the University of Washington School of Medicine, said during a presentation at the Cardiometabolic Health Congress. “The mechanisms for this are complex but appear to be related to specific beta cell toxicities, likely related from the ‘cytokine storm.’”
COVID-19 causes several metabolic and end-organ impacts. The release of cytokines can cause hepatocyte injury and impair glucose production, induce a stress response leading to more insulin resistance, and cause acute beta cell injury, Hirsch said.
Researchers are examining how SARS-CoV-2 is interacting with islets and affecting beta cells. A study published in Acta Diabetologica in 2010 discussed how the SARS coronavirus was able to enter islets using ACE2 as a receptor and damage them, causing acute diabetes. Hirsch noted while there are data both for and against ACE2 expression in beta cells, he believes SARS-CoV-2 might be able to damage them through a few different routes.
“Maybe it is more complicated than the ACE2 receptor,” Hirsch said. “Maybe there are other candidates when somebody is infected with COVID-19 that can cause beta cell toxicity. If we look at the beta cell as a whole, we know that in these infected individuals, interleukin-6 can cause the beta cell toxicity. We know there’s glucose toxicity from hyperglycemia, which we see both with and without preexisting diabetes. We know lipotoxicity with the high levels of free fatty acids, and of course, perhaps the ACE2 receptor itself. Maybe it’s a combination of these and not just COVID-19 and the ACE2 receptor itself.”
What is Double Diabetes? was written by Marissa Town for ChildrenWithDiabetes.com, 13 October 2021.
A recent publication in the journal BMC Endocrine Disorders looks at how obesity relates to double diabetes in adults with type 1 diabetes. Double diabetes is defined as having type 1 diabetes in combination with insulin resistance, which is the main feature of type 2 diabetes.2 It’s unclear exactly how prevalent this issue is for people with diabetes, so researchers in Bristol, United Kingdom reviewed the data for their patients who met the following criteria:
- Low C-peptide
- Two or more positive type 1 diabetes autoantibodies
- One positive t1d autoantibody + diagnosis age < 30 years
- History of DKA + diagnosis age < 30 years
- Diagnosed < 20 years of age regardless of autoantibody presence
To determine insulin resistance, they used a method called estimated glucose disposal rate (eGDR) and used the standard calculations to determine participants’ level of insulin resistance. This method was developed to use information from the person with diabetes including waist circumference, hypertension, weight, blood pressure, and more to calculate the risk of complications associated with insulin resistance.3 This also avoids the need to conduct the standard test for measuring insulin resistance, which is more invasive to the person with diabetes.
Read more: What is Double Diabetes?
Artificial sweeteners may cause digestive disease and discomfort was reported by Abigail Klein Leichman for Israel21c.org, 7 October 2021. New study finds aspartame, sucralose and saccharin interfere with bacterial communication in the gut.
Three years ago, Ben-Gurion University of the Negev Prof. Ariel Kushmaro revealed that these six sweeteners (aspartame, sucralose, saccharine, neotame, advantame and acesulfame potassium-k) are toxic to digestive gut microbes.
Now, he and colleagues from BGU and from Cyprus report in the International Journal of Molecular Sciences that three of these substances– aspartame, sucralose and saccharin – interfere with bacterial communication. And this, they theorize, could lead to digestive diseases and discomfort.
“The fact that bacteria use quorum sensing to communicate with each other revolutionizes our understanding and enables us to provide clearer answers,” said lead researcher Karina Golberg from BGU’s department of biotechnology engineering. “Artificial sweeteners disrupt that communication, which indicates that artificial sweeteners may be problematic in the long run,” said Golberg.