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Category: biotech/medical – Page 765

“Cancer” is not a word we want to hear. Conversations with your doctor about cancer can induce fear, anxiety, and a plethora of other emotions. But what if your doctor uses the phrase This terminology will probably still make a lot of people anxious and, in some situations, could result in some unnecessary treatment.

Several types of malignancies are associated with conditions that, while benign, could infer a more significant risk or likelihood of developing cancer in the future. Terminology including lesions, “stage 0” disease, or carcinoma “in situ” can all describe an abnormal, yet not malignant, finding. In addition to fear, these diagnoses can undoubtedly lead to patient confusion.

A diagnosis indicates abnormal cells present in a single location in the body. If a lesion isous, it has not spread to any other tissue, distant or nearby. This explains why theous conditions associated with several cancer types have names that involve the phrase “in situ,” which means “in its original place.”

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This is a bit technical. “nucleocytoplasmic compartmentalization assay”, Yeah buddy.

Life is dependent on the preservation and storage of information. The genome and epigenome are the two central storehouses of information in eukaryotes, and although they work interdependently, they are fundamentally quite different. Genetic information is consistent across all body cells throughout the life of an individual while epigenetic information varies between cells as well as changes over time and as per environment.

Researchers have identified several hallmarks of aging such as epigenetic alterations, genomic instability, cellular senescence, telomere attrition, mitochondrial dysfunction, and others [1]. These are known to play a role in the dysfunction and deterioration of cells with age. David Sinclair and other researchers have previously indicated that loss of epigenetic information can cause changes in gene expression, leading to cellular identity loss. Previous studies in mice have also shown that cell injuries such as cell crushing and DNA double-strand breaks can promote loss of epigenetic information which can accelerate aging along with age-related diseases [2].

Cellular senescence is a state of stable cell cycle arrest that can be triggered due to a wide range of extrinsic as well as intrinsic factors. It promotes tissue remodeling, wound repair, and cancer prevention by stopping the proliferation of damaged and aged cells. Senescent cells are characterized by metabolic and morphological alterations, reorganization of the chromatin, and release of pro-inflammatory substances known as the senescence-associated secretory phenotype (SASP) [3]. Irreparable DNA damage, loss of epigenetic information, and telomere shortening are a few factors that can initiate cellular senescence. Accumulation of senescent cells with age results in inflammation as well as the generation of reactive oxygen species (ROS).

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Continue reading “Did DunedinPACE Improve For Test #5 in 2023? Also, Is NAD Significantly Correlated With DunedinPACE?” | >

A research team led by Prof. Yossi Paltiel at the Hebrew University of Jerusalem with groups from HUJI, Weizmann, and IST Austria recently conducted a study unveiling the significant influence of nuclear spin on biological activities. This discovery challenges long-held assumptions and opens up exciting possibilities for advancements in biotechnology and quantum biology.

Scientists have long believed that nuclear spin had no impact on biological processes. However, recent research has shown that certain isotopes behave differently due to their nuclear spin. The team focused on stable oxygen isotopes (16O, 17O, 18O) and found that nuclear spin significantly affects oxygen dynamics in chiral environments, particularly in its transport.

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Centenarians, once considered rare, have become commonplace. Indeed, they are the fastest-growing demographic group of the world’s population, with numbers roughly doubling every ten years since the 1970s.

How long humans can live, and what determines a long and healthy life, have been of interest for as long as we know. Plato and Aristotle discussed and wrote about the ageing process over 2,300 years ago.

The pursuit of understanding the secrets behind exceptional longevity isn’t easy, however. It involves unravelling the complex interplay of genetic predisposition and lifestyle factors and how they interact throughout a person’s life.

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In this October 13 Learning Lab, Hilary Sherman, a Senior Scientist in the Corning Life Sciences Applications Lab, and Robert Padilla, a Field Application Scientist at Corning, dive into the topic of 3D culture techniques and why these technologies should be a part of any researcher’s repertoire.

Three-dimensional (3D) cultures such as spheroids and organoids are an important part of the research model market, helping to close the gap between cell cultures and animal models. Both organoids and spheroids have been used to create in vivo-like tissue models of cancer subtypes to study novel therapies and to make models for tissue engineering and regenerative medicine studies. But there are some key differences, with important implications for various applications. The right tool for a project is not always obvious. For spheroids and organoids, knowing where the cultures are similar and where they differ will help scientists select the best resource for their projects the first time around.

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Guidance and recommendations for prostate cancer screening have changed over the years. While there is no standard screening test, doctors may use a prostate-specific antigen (PSA) test to help diagnose prostate cancer. Doctors may follow a positive PSA test with a prostate biopsy.

Most recommending bodies emphasize a shared decision-making (SDM) approach for prostate cancer screening by PSA testing. This strategy moves away from doctors making treatment decisions and instead relies on collaborative interactions between patients and healthcare teams.

Why do expert opinions on prostate cancer screening differ? This remains a complex question with a lot to unpack. First, we have limited treatment options for cancer that has already spread outside of the prostate. Thus, detecting these cases will often not improve health or prolong life. Second, many cases of slow-growing prostate cancer will never become life-threatening; detection of these cases can be considered overdiagnosis and may lead to anxiety, unnecessary treatment, and accompanying side effects. Unnecessary biopsies, which provide no additional value to patients and physicians in decision-making, can also come with complications such as bleeding and infection.

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New research that helps explain the molecular processes involved in the painful autoimmune disease ankylosing spondylitis, or AS, may reduce the guessing game that health care providers currently play while attempting to treat the condition.

A team from Oregon Health & Science University and the VA Portland Health Care System has found a specific kind of AS treatment that is effective when used by patients who have a particular genetic mutation. Their study was published today in the journal Annals of the Rheumatic Diseases, and its findings could lead to more targeted, timely and patient-specific treatment recommendations.

“This is the first time research has shown that we might be able to use genetic markers to determine which therapy ankylosing spondylitis patients should receive,” said the study’s senior researcher, Ruth Napier, Ph.D., assistant professor of molecular microbiology and immunology, arthritis and rheumatic in the OHSU School of Medicine, and principal investigator with VA Portland. “These promising findings are encouraging. This is the first time I can say that I’m on the cusp of making a difference for patients with ankylosing spondylitis who seek relief.”

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