Category Archives: Biochemistry

NEW ORLEANS The Men's and Women's Scholar-Athlete of the Year and All-Academic Athletes for the 2021 NCAA Division III Cross Country season were announced on Thursday by the U.S. Track & Field and Cross Country Coaches Association (USTFCCCA).

Both the men's and women's cross country teams earned USTFCCCA All-Academic Team honors, with the men's team recording a cumulative team GPA of 3.2, while the women's team recorded an impressive 3.59 cumulative GPA.

For the women's team, three Knights were awarded All-Academic Athletes, consisting of Bayleigh Redd, Sasha Willie, and Ashley Brewer, majoring in Biochemistry.Quin Meyer, majoring in Business Management, and Kaelen Ruder, majoring in Physical Therapy, represented the men's team.

The group played key roles for their teams in their 2021campaigns, finishing in the top 25 percent at the 2021 NCAA Division III South Region Cross Country Championships. Their performances, along with their academic achievements, qualified themselves for USTFCCCA All-Academic Awards.

Follow @knightxctf on Instagram and Twitter for more updates and details on the team.

Full USTFCCCA Release

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Men's and Women's Cross Country Earn All-Academic Honors - Southern Virginia - Southern Virginia University News

The Latest released Global Biochemical Oxygen Demand Analyzer Market Report 2021-2027 provides 100+ data Tables, Pie Chat, Graphs & Figures spread through Pages and easy to understand detailed analysis.

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This research, led by Jean Cook, PhD, and Liu Mei, PhD, at the UNC School of Medicine, may help explain why certain parts of the genome become highly mutable in some cancers.

CHAPEL HILL, NC A new study from scientists at the UNC School of Medicine has illuminated an important process that occurs during cell division and is a likely source of DNA damage under some circumstances, including cancer.

The scientists, who reported their findings in Nucleic Acids Research, devised a sophisticated experimental platform for studying the process called origin licensing. Cells use this process to regulate, or license the replication of their genomes during cell division.

The researchers revealed for the first time the dynamics of this process. They showed in particular how these dynamics differ and bring different risks of DNA damage during replication in the two basic states of genomic DNA, the euchromatin state which is relatively loose and open for gene activity, and the heterochromatin state which is wound more tightly to silence gene activity.

Our findings may help explain, for example, why certain portions of the genome are relatively susceptible to DNA damage during replication in some cancer cells, said study senior author Jean Cook, PhD, professor of biochemistry and biophysics at the UNC School of Medicine and member of the UNC Lineberger Comprehensive Cancer Center.

Origin licensing occurs in the initial, preparatory phase of cell replication, known as the G1 phase. It involves sets of special enzymes that attach to the DNA in chromosomes at various locations where DNA-copying is to originate. The enzymes essentially license the copying of DNA so that cells dont copy their genomes more than once.

Cook and other scientists have described in prior studies the basic process of origin licensing, and have identified proteins that make it happen. But this study, for the first time, revealed in detail how the process unfolds over time in cells as they prepare for cell division. Study first author Liu Mei, PhD, a postdoctoral fellow in the Cook laboratory, combined still and time-lapse microscopic imaging techniques to accomplish this feat.

What Liu did was incredibly painstaking and meticulous, a technical tour de force, Cook said.

As an initial demonstration of her experimental platform, Mei compared the origin licensing process, with its loading of licensing enzymes, in the two main states of the genome euchromatin and heterochromatin. She found an important difference.

Essentially heterochromatin more compacted DNA loads these licensing enzymes relatively late compared to what we observe in the more open euchromatin, Mei said.

This finding hinted, at least, that in dividing cells with an abnormally shortened G1 phase, the more compacted DNA in the cell genome might never be fully licensed for replication, potentially resulting in large mutations during replication and even cell death. Confirming this possibility, the researchers found that when they artificially shortened the G1 phase in test cells, there was significantly more under-replication and DNA damage in heterochromatin regions of the cells genomes, compared to the euchromatin regions.

Cells can have a shortened G1 phase for different reasons, including due to cancer. Thus the study suggests that the genomic instability or tendency to develop more mutations of some cancer types, as well as the genomic locations of that instability, might be explained in part by faulty origin licensing.

The study also establishes the researchers experimental platform as a tool for further studies of origin licensing dynamics and genomic instability, studies that might someday yield new strategies against cancers, for example.

The consequences of differential origin licensing dynamics in distinct chromatin environments was co-authored by Liu Mei, Katarzyna Kedziora, Eun-Ah Song, Jeremy Purvis, and Jean Cook, all at UNC Chapel Hill.

Funding was provided by the National Institutes of Health (R01GM102413, R01GM083024, R35GM141833, R01-GM138834).

Media contact: Mark Derewicz, 919-923-0959.

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Ground-Breaking Study Reveals Dynamics of DNA Replication 'Licensing' | Newsroom - UNC Health and UNC School of Medicine

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Growth Drivers of Colistin Sulphate Market with Relevancy Mapping by Key Player like Shengxue Dacheng, Apeloa, Livzon Group, LKPC, Xellia, Qianjiang...

It is controversial whether viruses are alive, but they do evolve like all living things. This fact has become abundantly clear during the pandemic, as new variants of concern have emerged every few months.

Some of these variants have been better at spreading from person to person, eventually becoming dominant as they out-compete slower versions of SARS-CoV-2, the virus that causes COVID-19. This improved spreading ability has been ascribed to mutations in the spike protein the mushroom-shaped projections on the surface of the virus that allow it to bind more strongly to ACE2 receptors.

ACE2 are receptors on the surface of our cells, such as those that line our airways, that the virus attaches to in order to gain entry and start replicating. These mutations allowed the alpha variant, and then the delta variant, to become globally dominant. And scientists expect the same thing to happen with omicron.

The virus cannot, however, improve indefinitely. The laws of biochemistry mean that the virus will eventually evolve a spike protein that binds to ACE2 as strongly as possible. By that point, the ability of SARS-CoV-2 to spread between people will not be limited by how well the virus can stick to the outside of cells. Other factors will limit virus spread, such as how fast the genome can replicate, how quickly the virus can enter the cell via the protein TMPRSS2, and how much virus an infected human can shed. In principle, all of these should eventually evolve to peak performance.

Has omicron reached this peak? There is no good reason to assume that it has. So-called gain-of-function studies, which look at what mutations SARS-CoV-2 needs to spread more efficiently, have identified plenty of mutations that improve the spike proteins ability to bind to human cells that omicron does not have. Besides this, improvements could be made to other aspects of the virus life cycle, such as genome replication, as I mentioned above.

But assume for a second that omicron is the variant with maximized spreading ability. Perhaps omicron will not get any better because it is limited by genetic probability. In the same way that zebras have not evolved eyes at the back of their heads to avoid predators, it is plausible that SARS-CoV-2 cannot pick up the mutations required to reach a theoretical maximum as those mutations need to occur all at once, and that is just too unlikely to emerge. Even in a scenario where omicron is the best variant at spreading between humans, new variants will emerge to handle the human immune system.

After infection with any virus, the immune system adapts by making antibodies that stick to the virus to neutralize it, and killer T-cells that destroy infected cells. Antibodies are pieces of protein that stick to the specific molecular shape of the virus, and killer T-cells recognize infected cells via molecular shape as well. SARS-CoV-2 can therefore evade the immune system by mutating sufficiently that its molecular shape changes beyond the immune systems recognition.

This is why omicron is so apparently successful at infecting people with previous immunity, either from vaccines or infections with other variants the mutations that allow the spike to bind to ACE2 more strongly also reduce the ability of antibodies to bind to the virus and neutralize it. Pfizers data suggests that T-cells should respond similarly to omicron as to previous variants, which aligns with the observation that omicron has a lower fatality rate in South Africa, where most people have immunity.

Importantly for humanity, past exposure still seems to protect against severe disease and death, leaving us with a compromise where the virus can replicate and reinfect, but we do not get as severely sick as the first time.

Probable future

Herein lies the most probable future for this virus. Even if it behaves like a professional gamer and eventually maxes out all its stats, there is no reason to think that it will not be controlled and cleared by the immune system. The mutations that improve its spreading ability do not greatly increase deaths. This maxed-out virus would then simply mutate randomly, changing enough over time to become unrecognizable to the immune systems adapted defenses, allowing waves of reinfection.

We might have COVID season each winter in the same way we have flu season now. Influenza viruses can also have a similar pattern of mutation over time, known as antigenic drift, leading to reinfections. Each years new flu viruses are not necessarily better than last years, just sufficiently different. Perhaps the best evidence for this eventuality for SARS-CoV-2 is that 229E, a coronavirus that causes the common cold, does this already.

Omicron will therefore not be the final variant, but it may be the final variant of concern. If we are lucky, and the course of this pandemic is hard to predict, SARS-CoV-2 will probably become an endemic virus that slowly mutates over time.

The disease might very likely be mild as some past exposure creates immunity that reduces the likelihood of hospitalization and death. Most people will get infected the first time as a child, which could occur before or after a vaccine, and subsequent reinfections will barely be noticed. Only a small group of scientists will track SARS-CoV-2s genetic changes over time, and the variants of concern will become a thing of the past at least until the next virus jumps the species barrier.

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Beyond Omicron: The laws of biochemistry mean that COVID-19 variants cannot improve indefinitely - Milwaukee Independent

The biochemistry of vision is a complex process. The molecules supporting the visual pigments that allow us to see our surrounding reality have remained essentially invisible for scientists for a long time. The team led by Prof. Maciej Wojtkowski from the International Centre for Translational Eye Research (ICTER) has changed that, thanks to an innovative state-of-the art imaging device that they have developed.

It is commonly said that eyes are the mirror of the soul; however, they are undoubtedly our window on the world. The retina of the eye represents the first and very important processing station for the path of light as it is converted into an image. Molecular reactions occurring in the retina are crucial for the perception of visual stimuli from the environment.

For many years scientists and doctors have not been able to observe molecules present in the natural milieu of the retinal photosensitive cellsin vivo. The team of scientists led by Prof. Maciej Wojtkowski from ICTER at theInstitute of Physical Chemistry, Polish Academy of Sciences(IPC PAS) have developed a two-photon excited fluorescence scanning laser ophthalmoscope (TPEF-SLO). It is an instrument that remarkably allows viewing the biochemistry of vision in the living eye in real time. Prof. Wojtkowski points out that thanks to close collaborations with biochemist Prof. Kris Palczewski from the University of California Irvine and the laser group of Prof. Grzegorz Sobo from the Wrocaw University of Science and Technology, we can quickly and effectively demonstrate the capabilities of the new imaging method and validate its utility for diagnosing disease progression and treatment, leading to its use in clinical practice.

The human eye is one of the most precise organs of our body, capable of distinguishing about 200 pure colors. Mixing these colors produces about 17,000 different hues, and taking into account our ability to distinguish about 300 intensities of color associated with light intensity, we get a staggering 5 million perceived colors.

The retina, the part of the eye that receives visual stimuli, contains photosensitive cells, cones and rods. The cones enable us to see and distinguish colors in bright light, while the rods are sensitive to single pulses of visible light at dusk or night. Visual impressions are transmittedviathe optic nerve to the primary visual cortex in the brain, but the signals that carry the visual impressions are the result of biochemical processes that occur in the photoreceptors. Simplifying, we can say that the human eye is a biochemical factory whose activity depends on biochemical transformations of a single molecule, retinal. This molecule is indispensable for the function of the visual pigments, namely rhodopsin in rods says Prof. Maciej Wojtkowski.

Rhodopsin, the visual pigment in rods is a light sensitive G-protein coupled receptor (GPCR). Absorption of a quantum of radiation causes isomerization of 11-cis-retinal within the rhodopsin binding pocket and subsequent hyperpolarization of the photoreceptor membranes. In this manner the visual impulse is initiated and transmitted to the brain. A deficiency of vitamin A, precursor of retinal, reduces the ability to see at night, known as night blindness or nyctalopia.

Unfortunately, the molecules indispensable for sustaining visual pigments are undetectable by scientific instruments during virtually the entire visual cycle in living humans. However, there is one instant in the visual cycle when the molecules can be seen; we cant detect them with UV light, but we can observe them thanks to so-called fluorescence with two-photon excitation, adds Dr. Jakub Boguslawski, a main researcher on the project.

Ophthalmic imaging techniques are fundamental in diagnosing retinal pathologies. With optical tomography (OCT), scanning laser ophthalmoscopy (SLO), and fundus autofluorescence, we have made advances in understanding mechanisms of eye diseases. This collection of advanced technologies, however, is an insufficient arsenal for full insight into the chemistry of vision. Non-invasive assessment of metabolic processes occurring in retinal cells (visual pigment regeneration) is essential for the development of future therapies. In the case of age-related macular degeneration (AMD), which is one of the most common diseases causing blindness, cells within a disease-altered retina cannot be distinguished at an early stage from cells of a normal healthy retina. However, the differences can be picked up by biochemical markers, if these markers can be fluorescently induced.

This is the idea behind two-photon fluorescence imaging (TPE). It is an advanced technique for measuring compounds that support the function of visual pigments and are not visible in other tests.

Compared to traditional imaging methods based on single-photon fluorescence, TPE allows the metabolites of vitamin A that are involved in vision, such as retinol or retinol esters, to be viewed. The eye is an ideal organ for multiphoton imaging, says Prof. Wojtkowski, whose team is responsible for the discovery. Eye tissues such as the sclera, cornea, and lens are highly transparent to near-infrared light. This, in turn, penetrates retinal tissues in a non-invasive way.

Images obtained with TPEF-SLO have confirmed that this is an effective way to view the molecules that sustain visual function. Comparison of data from humans with retinal degeneration with mouse models of the disease revealed a similar rapid accumulationof bisretinoid condensation products. We believe that visual cycle intermediates and toxic byproducts of this metabolic pathway could be measured and quantified using TPE imaging, says Dr. Grazyna Palczewska, one of the projects main investigators.

This new age instrument, enabling non-invasive assessment of the metabolic state of the human retina, opens numerous therapeutic possibilities for degenerative diseases of the retina, including the testing of new drugs. By understanding the biochemistry of vision and the alterations that occur in disease, physicians will be able to pinpoint precise locations of the lesions and assess the impact of therapy. The research on TPEF-SLO was published inThe Journal of Clinical Investigation.

Reference:Boguslawski J, Palczewska G, Tomczewski S, et al. In vivo imaging of the human eye using a two-photon excited fluorescence scanning laser ophthalmoscope. J Clin Invest. 2021. doi:10.1172/JCI154218

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Seeing the Chemistry of Vision - Technology Networks