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Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 11:57am

One non-invasive method is imagery rehearsal therapy, in which patients rewrite their most harrowing and frequent nightmares to give them a happy ending. Then, they "rehearse" telling themselves that rewritten story, trying to overwrite the nightmare.

This method can reduce the frequency and severity of nightmares, but the treatment is not effective for all patients.

In 2010 scientists found that playing sounds that people have been trained to associate with a certain stimulus, while those people are sleeping, aids in boosting the memory of that stimulus. This has been named targeted memory reactivation (TMR), and researchers wanted to find out if it could improve the effectiveness of imagery rehearsal therapy (IRT).

After having the study's participants complete a dream and sleep diary for two weeks, the volunteers were all given a single IRT session. At this point, half of the group underwent a TMR session, creating a link between a positive version of their nightmares and a sound.

The other half served as a control group, imagining a less horrific version of a nightmare without being exposed to positive sounds.

Both groups received a sleep headphone headband that would play the sound – the piano chord C69 – while they were sleeping, every 10 seconds during REM sleep when nightmares were most likely to occur.

The groups were evaluated after two weeks of additional diary entries, and then again after three months without any sort of treatment.

At the start of the study, the control group had, on average, 2.58 nightmares per week, and the TMR group had an average of 2.94 weekly nightmares. By the end of the study, the control group was down to 1.02 weekly nightmares, while the TMR group had dropped to just 0.19. Even more promising, the TMR group reported an increase in happy dreams.

Part 2

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 11:56am

Nightmares Can Be Silenced by a Single Piano Chord, Scientists Find

Using non-invasive techniques to manipulate our emotions, it might be possible to curtail the screaming horrors that plague our sleep.

A study last year conducted on 36 patients diagnosed with a nightmare disorder showed that a combination of two simple therapies reduced the frequency of their bad dreams.

Scientists invited the volunteers to rewrite their most frequent nightmares in a positive light and then played sound associated with positive experiences as they slept.

"There is a relationship between the types of emotions experienced in dreams and our emotional well-being. Based on this observation, sceintists had the idea that they could help people by manipulating emotions in their dreams. In this study, they show that they can reduce the number of emotionally very strong and very negative dreams in patients suffering from nightmares.

Many people suffer from nightmares, which aren't always a simple case of a few bad dreams. Nightmares are also associated with poor-quality sleep, which in turn is linked with a whole plethora of other health issues.

Poor sleep can also increase anxiety, which in turn can result in insomnia and nightmares. Recent studies have shown that nightmares and sleep disturbances have seen an uptick during the ongoing global SARS-CoV-2 pandemic.

Given that we don't really understand why, or even how, our brain creates dreams while we sleep, treating chronic nightmares is something of a challenge.

Part 1

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 11:52am

Why should our PC or laptop  restart to install updates?

Software comprises lots of files and programs all interacting. 

When a computer is running software, it loads much of the program into its memory.

If we managed to update that same software on the hard disk or solid state drive (SSD), then the program may panic as everything will be different – it won’t be able to find the files that were there a moment ago. The version in memory will not be compatible with the version on the hard disk or SSD. Lots of errors will be thrown and your computer may crash.

To prevent this, operating systems usually insist that when major updates are needed, we shut down the software being updated, then restart with the new software installed.

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 11:00am

The Human Digestive System Varies a lot from person to person

The human digestive system is much more variable than we tend to think, according to a new study, with significant differences in gut anatomy even among healthy individuals.

This includes individual differences from person to person, the researchers report, plus broader differences such as those between women and men.

In one noteworthy example, the researchers found that women tend to have longer small intestines than men, by an average of 30.7 centimeters.

Because having a longer small intestine helps you extract nutrients from your diet, this finding supports the canalization hypothesis, which posits that women are better able to survive during periods of stress.

The study also revealed more granular differences, suggesting healthy human digestive systems are far more variable than many experts had appreciated.

If you're talking to four different people, odds are good that all of them have different guts, in terms of the relative sizes of the organs that make up that system.

For example, the cecum is an organ that's found at the nexus of the large and small intestine[s]. One person may have a cecum that is only a few centimeters long, while another may have a cecum the size of a coin purse.

The researchers point out that this has big implications for health care, emphasizing the importance of recognizing individual differences in gastrointestinal systems rather than focusing on typical or "normal" anatomy among humans in general.

The researchers point out, however, that humans stand apart for our high variation in intestinal length compared with other species. One possible explanation, they suggest, is that humans don't eat a "standardized captive diet," unlike many other species .

https://peerj.com/articles/15148/

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 10:52am

9. W. Huang et al., "Cellular senescence: the good, the bad and the unknown," Nat Rev Nephrol, 18(10):611-27, 2022. 

10. D. McHugh, J. Gil, "Senescence and aging: causes, consequences, and therapeutic avenues," J Cell Biol, 217(1):65-77, 2018.  

11. R. Di Micco et al., "Cellular senescence in ageing: from mechanisms to therapeutic opportunities," Nat Rev Mol Cell Biol, 22(2):75-95, 2021.

12. J. Yang et al., "The paradoxical role of cellular senescence in cancer," Front Cell Devl Biol, 9, 2021. 

13. F. Hernandez-Gonzalez et al., "Cellular senescence in lung fibrosis," Int J Mol Sci, 22(13):7012, 2021. 

14. A.K. Palmer et al., "Senolytics: potential for alleviating diabetes and its complications," Endocrinology, 162(8):bqab058, 2021. 

15. D. Beaulieu et al., "Phospholipase A2 receptor 1 promotes lung cell senescence and emphysema in obstructive lung disease. Euro Respir J, 2021. 

Part 5

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Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 10:51am

Footnotes:

 J. Park et al., "Promotion of intestinal epithelial cell turnover by commensal bacteria: role of short-chain fatty acids," PLoS ONE, 11(5):e0156334, 2016. 

2. L. Ottoboni et al., "Therapeutic plasticity of neural stem cells," Front Neurol, 11, 2020.  

3. L. Hayflick, P.S. Moorhead, "The serial cultivation of human diploid cell strains," Exp Cell Res, 25(3):585-621, 1961.

4. Kumari R, Jat P. "Mechanisms of cellular senescence: cell cycle arrest and senescence associated secretory phenotype," Front Cell Dev Biol, 2021.

5. V. Gorgoulis et al., "Cellular senescence: defining a path forward," Cell, 179(4):813-27, 2019.  

6. N.S. Gasek et al., "Strategies for targeting senescent cells in human disease," Nat Aging, 1(10):870-79, 2021. 

7. S. Da Silva-Álvarez et al., "The development of cell senescence," Exp Gerontol, 128:110742, 2019. 

8. M. Storer et al., "Senescence Is a developmental mechanism that contributes to embryonic growth and patterning," Cell, 155(5):1119-30, 2013.  

Part 4

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 10:51am

Anti-senescent Treatments

Researchers have developed drugs called senolytics to selectively target senescent cells that are resistant to apoptosis. These drugs work by upregulating antiapoptotic pathways.⁶ Eliminating these cells is important in diseases such as fibrosis (e.g., pulmonary fibrosis), where tissue is scarred and thickened.¹³ Additionally, patients with obesity or diabetes have high levels of senescent cells in adipose tissue, which contributes to fat cell size.¹⁴ For pulmonary fibrosis and diabetic kidney disease, researchers have conducted clinical trials testing senolytics and observed promising results.⁶

Another class of drugs called senomorphics inhibits SASP.⁶ Reducing SASP is critical for preventing the spread of senescence to neighboring cells or tissues. For example, ruxolitinib reduces inflammation by inhibiting Janus kinases (JAKs), proteins involved in cytokine production.⁹ This drug was shown to be an effective treatment in a chronic obstructive pulmonary disease mouse model.¹⁵

^{Part 3}

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 10:51am

What Triggers Cell Senescence? 
Cell senescence is triggered by a variety of internal or external cellular insults. Examples of internal stresses leading to senescence include shortening of the telomeres, DNA damage, mitochondrial dysfunction, nutrient deprivation, oncogenic pathway activation.⁴ Some examples of external stresses are radiation and chemotherapeutic agents.⁴  

Senescence-Associated Secretory Phenotype 
A major characteristic of senescent cells is the senescence-associated secretory phenotype or SASP.¹⁰ SASP encompasses a senescent cell’s secreted components, or secretome, and includes pro-inflammatory cytokines, chemokines, proteases, growth factors, reactive oxygen species (ROS), and extracellular matrix proteins.¹⁰ Senescent cells use these metabolically active components to communicate with surrounding cells and change the environment in either a positive or negative manner. For instance, SASP can recruit immune cells to remove senescent cells, remodel tissue by secreting angiogenic factors, or promote senescence in other cells through paracrine signalling.¹⁰

Senescence and Aging 

Senescence is an important contributor to aging as it depletes various cell pools, including progenitor and stem cells that can replace damaged tissue over time.¹¹ The SASP of senescent cells enhances inflammation, which increases susceptibility to many age-related diseases, such as heart disease, diabetes, and cancer.¹¹ SASP-mediated paracrine signaling can also encourage neighboring cells to undergo senescence.¹¹

Senescence and Cancer 

A major hallmark of cancer progression is cell proliferation.³ As such, researchers previously thought that the senescence pathway suppressed tumors as it eliminated proliferative cells.¹² However, there is increasing evidence that the SASP may contribute to cancer progression by creating an immunosuppressive environment.¹²

^{Part 2}

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 10:50am

Cell Senescence

Each cell in an organism has an average life span. For example, cells lining the surface of the human gut or skin typically live 3-5 days before they die.¹ In contrast, stem cells and neurons can survive for many years.² The process by which a cell arrests their growth after completing its life span is called cell senescence.  

Cell senescence is the expression of aging at the cellular level, and the phenomenon occurs when a cell stops dividing and arrests in the G1 phase of the cell cycle.^3,4 During this phase, the cell undergoes numerous phenotypic and metabolic changes. Some of these phenotypic changes include chromatin remodeling with global demethylation and heterochromatin foci formation, which alters the cell’s gene expression landscape.⁵ Additionally, senescent cells are larger in size and more granular.⁶ Senescent cells are eradicated from the body either through apoptosis or by immune cells such as macrophages.⁵

Although cell senescence is often associated with aging, it is an important process during embryogenesis, wound healing, and maintaining homeostasis.⁷ For instance, during central nervous system development, parts of the neural tube undergo senescence for proper formation of the brain and spinal cord.⁸

Cell senescence was first identified by Leonard Hayflick and Paul Moorhead in 1961, when they serially passaged human fibroblast cells in culture.³ They noticed that the cells stopped dividing after 40-60 passages. The number of cell divisions before cell cycle arrest is now known as the Hayflick limit.³

To detect senescent cells in the laboratory, researchers use markers such as senescence-associated B-galactosidase (SABG), which exists in the lysosome of these cells.⁹

^{Part 1}

Comment by Dr. Krishna Kumari Challa on May 7, 2023 at 10:44am

Mechanical Force on the Skull May Aid Bone Regeneration

By mechanically inducing the expansion of cranial sutures in young adult mice, researchers stimulated stem cell proliferation that is key to healing bone injuries.

Treatments available to repair damage to the skull as a result of trauma, surgery, or congenital anomalies are limited and sometimes involve risks. A study recently published in PNAS (1) offers an alternative approach inspired by how babies regenerate bone tissue. The researchers expanded on previous studies (2,3) showing that open sutures—the fibrous connective tissue holding bones together—in the skulls of newborn mice and humans are reservoirs of skeletal stem cells. The temporary mechanically-induced expansion of closed sutures in young adult mice resulted in the proliferation of skeletal stem cells and facilitated bone regeneration following an injury.

A major contribution of this study is that it advances our knowledge about the impact of external forces on the structure of cranial sutures and the potential healing properties of such impact.

Researchers first compared the cell composition of the calvarial suture—which joins the bilateral bones in the roof of the skull—in mice of different ages and found that the number of skeletal stem cells is significantly reduced in older mice compared to younger mice. Increased numbers of stem cells correlate with open sutures in newborns, leading them to wonder whether expanding the sutures in adults would increase the number of stem cells enough to harness their regenerative potential.

The team achieved this goal in 2-month-old mice, which the researchers considered the equivalent of young adults in humans. When the researchers mechanically induced calvarial suture expansion, the number of skeletal stem cells increased significantly. Moreover, mice that received an injury to the skull near the suture simultaneous to the mechanical expansion exhibited near complete bone regeneration after 60 days, something that was not achieved in control mice without the expansion device. This mechanically-induced regeneration did not occur in 10-month-old mice, probably due to the limited supply of preexisting skeletal stem cells in the sutures, which is insufficient to achieve successful proliferation.

Finally, the team showed that suture stem cell proliferation and the resulting healing effects depend on Wnt signaling, a pathway that regulates key aspects of animal development.

1. Aldawood, Z.A. et al. (2023) “Expansion of the sagittal suture induces proliferation of skeletal stem cells and sustains endogenous calvarial bone regeneration,” Proceedings of the National Academy of Sciences

2. Zhao, H. et al. (2015) “The suture provides a niche for mesenchymal stem cells of Craniofacial Bones,” Nature Cell Biology, 17(4), pp. 386–396. Available at: https://doi.org/10.1038/ncb3139.

3. Maruyama, T. et al. (2016) “Stem cells of the suture mesenchyme in craniofacial bone development, repair and Regeneration,” Nature Communications, 7(1). Available at: https://doi.org/10.1038/ncomms10526.

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