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How light suppresses virulence in an antibiotic-resistant pathogen

Light is a universal stimulus that influences all living things. Cycles of light and dark help set the biological clocks for organisms ranging from single-celled bacteria to human beings. Some bacteria use photosynthesis to convert sunlight into energy just like plants, but other bacteria sense light for less well-known functions.

In 2019, Sampriti Mukherjee, Ph.D., and her team at the University of Chicago discovered that far-red light, part of the light spectrum near the infrared range, prevents the formation of biofilms by the human pathogen Pseudomonas aeruginosa.

Biofilms form when communities of bacteria cluster together and attach to surfaces like medical devices or tissues. Pseudomonas aeruginosa is an antibiotic-resistant bacterium, normally found in the soil and water, that is known to cause difficult to treat infections in hospitalized patients, especially those with weakened immune systems, lung diseases, or large wounds like burns. Figuring out how to prevent this pathogen from forming biofilms could help treat these dangerous infections.

AI-driven ultrafast spectrometer-on-a-chip advances real-time sensing

For decades, the ability to visualize the chemical composition of materials, whether for diagnosing a disease, assessing food quality, or analyzing pollution, depended on large, expensive laboratory instruments called spectrometers. These devices work by taking light, spreading it out into a rainbow using a prism or grating, and measuring the intensity of each color. The problem is that spreading light requires a long physical path, making the device inherently bulky.

A recent study from the University of California Davis (UC Davis), reported in Advanced Photonics, tackles the challenge of miniaturization, aiming to shrink a lab-grade spectrometer down to the size of a grain of sand, a tiny spectrometer-on-a-chip that can be integrated into portable devices. The traditional approach of spatially spreading light is abandoned in favor of a reconstructive method.

Instead of physically separating each color, the new chip uses only 16 distinct silicon detectors, each engineered to respond slightly differently to incoming light. This is analogous to giving a handful of specialized sensors a mixed drink, with each sensor sampling a different aspect of the drink. The key to deciphering the original recipe is the second part of the invention: artificial intelligence (AI).

DNA Breakthrough Solves Decade-Old Mystery of the Beachy Head Woman

New research suggests the mysterious Roman-era “Beachy Head Woman” was likely from Britain, not the Mediterranean or sub-Saharan Africa. Advances in DNA sequencing are helping researchers resolve a mystery that has surrounded the Beachy Head Woman for more than ten years. The remains of a youn

Elite army training reveals genetic markers for resilience

A new analysis of soldiers attempting to join the U.S. Army Special Forces suggests that specific genetic variations play a role in how individuals handle extreme physical and mental pressure. The research identified distinct links between a soldier’s DNA and their cognitive performance, psychological resilience, and physiological stress response during a grueling selection course. These findings were published recently in the academic journal Physiology & Behavior.

To become a member of the elite Army Special Forces, a soldier must first pass the Special Forces Assessment and Selection course. This training program is widely recognized as one of the most difficult military evaluations in the world. Candidates must endure nearly three weeks of intense physical exertion. They face sleep deprivation and complex problem-solving exercises. The attrition rate is notoriously high. Approximately 70 percent of the soldiers who attempt the course fail to complete it. This environment creates a unique laboratory for scientists to study human endurance.

Researchers have sought to understand why some individuals thrive in these punishing environments while others struggle. Resilience is generally defined as the ability to adapt positively to adversity, trauma, or threats. It involves a combination of psychological stability and physiological recovery. While physical training and mental preparation are essential, biological factors also play a substantial role. Genetics help determine how the brain regulates chemicals and how the body processes stress hormones.

Over 60 THIS Morning Habit TRIPLES Stroke Risk In Older Adults!

Over 60? THIS Morning Habit TRIPLES Stroke Risk In Older Adults! | Senior Health Tips.

Most people don’t know this, but the first 90 minutes after waking are the most dangerous for adults over 60 — especially when it comes to stroke risk. 🧠⚠️ New studies from Harvard, Tokyo, and Toronto reveal that certain common morning habits can dramatically increase vascular stress, spike blood pressure, restrict blood flow to the brain, and trigger dangerous clotting patterns in older adults. These habits look harmless on the outside, but inside the body, they create the perfect storm for a stroke. 😳

In this video, we reveal the 6 morning habits that triple stroke risk in seniors, ranked from least to most dangerous. You’ll learn why the aging vascular system reacts differently in the morning, why certain actions overload the arteries, how sudden pressure changes affect the brain, and the specific morning routines neurologists now warn older adults to avoid. We also explain what the research discovered about Habit #1 — a behavior so strongly linked to stroke risk that scientists repeated the study twice to confirm the results. 🧬📊

If you or someone you love is over 60, this is essential information. These morning habits can quietly raise your risk without symptoms, but the good news is that simple changes can help protect your brain, improve circulation, and lower your chances of experiencing a life-altering event. ❤️‍🩹 Stay until the end — your brain health may depend on it.

⌛Timestamps:
⏱️ Intro – 00:00
⚠️ Habit No.5 – 02:36
⚠️ Habit No.4 – 05:57
⚠️ Habit No.3 – 09:24
⚠️ Habit No.2 – 13:30
⚠️ Habit No.1 – 17:54

#SeniorHealth #SeniorHealthTips #SeniorWellness #SeniorZone #StrokeRisk #StrokePrevention #MorningHabits #Over60Health #BrainHealth #HealthyAging #SeniorSafety #HighBloodPressure #CirculationHealth #AgingWell #UnitedStates #Wisdom #NeurologyTips #SeniorCare #VascularHealth #HealthyMorningRoutine #LongevityTips.

Aberrant Complement Activation Is a Prominent Feature of Chronic Inflammatory Demyelinating Polyneuropathy

To comprehensively characterize complement pathway activation in chronic inflammatory demyelinating polyneuropathy (CIDP) and its association with clinical disease features using advanced complement profiling.

B cells play a more sinister role than believed in progression of type 1 diabetes

A recent study by Vanderbilt Health researchers has revealed a greater, detrimental role for B lymphocytes (B cells) in the progression of type 1 diabetes (T1D).

B cells are immune cells thought to drive the immune system’s attack on insulin-producing beta cells by activating anti-islet T cells. The study published in Diabetes suggests they play an even more sinister role by also interfering with and limiting the function of regulatory T cells (Tregs) that help calm the immune system.

“Our study showed B cells can weaken the body’s natural defenses by interfering with Tregs, which normally behave as peacekeepers to ward off immune attacks on the pancreas and the insulin-producing beta cells,” said Daniel Moore, MD, PhD, associate professor of Pediatrics at Vanderbilt Health and the study’s corresponding author.

MCM8- and MCM9 Deficiencies Cause Lifelong Increased Hematopoietic DNA Damage Driving p53-Dependent Myeloid Tumors

(Cell Reports 28, 2851–2865.e1–e4; September 10, 2019)

Our attention was called to an image duplication in the right panel of Figure 3C in our published paper. Note that the right panels are not new results but enlarged representative cases present in the left panel, as indicated in the figure legend. They show so-called Howell-Jolly bodies (faulty, dysplastic red blood cells that did not manage to expulse their cell nucleus completely). The first and second images show the same cell in question but in different clippings. We apologize for this inadvertent mistake and provide a revised Figure 3C depicting a fifth example of (two) erythrocytes displaying Howell-Jolly bodies in the right panel.

Intestinal epithelial TLR5 signaling promotes barrier-supportive macrophages

Crosstalk between commensal E. coli that express flagellin and intestinal epithelial cells coordinate intestinal macrophage recruitment to support gut barrier homeostasis in mice.

Learn more in ScienceImmunology.


The colonic epithelium is an important boundary between internal tissues and luminal contents including the microbiota. The gut microbiota drives immune cell accumulation and effector function (6, 10, 12), but how colonic epithelial cells mediate these processes is incompletely understood. To understand how intestinal epithelial sensing of adherent microbes regulates immune-supported intestinal barrier repair, we used the E. coli strain 541–15, which we previously found increased LP macrophages and promoted their IL-10 production, protecting against inflammatory pathology in mouse colitis models (12, 23, 24).

Here, we demonstrated that E. coli 541–15 colonization promotes LP recruitment of mature macrophages after antibiotic treatment. Using HCMs, we determined that E. coli 541–15 induced expression of immune regulatory genes including the monocyte-recruiting chemokine CCL2 exclusively in UD cells, which promote monocyte migration. In vivo, CCL2 produced by epithelial cells in response to E. coli 541–15 colonization promoted colon LP macrophage expansion and protected mice from DSS colitis. We further identified flagellin as the key microbial factor that induced epithelial CCL2 expression. Last, epithelial TLR5 and E. coli flagellin were both required for LP recruitment of mature macrophages and protection against DSS challenge. In both in vitro and in vivo systems, epithelial stem cells had higher TLR5 expression than mature IECs, indicating a crypt specific role for flagellated bacteria detection. Our findings are consistent with previous studies showing that TLR5-deficient mice develop spontaneous colitis in the presence of the pathobiont H. hepaticus (20), suggesting a potential protective role for TLR5 in intestinal homeostasis. Moreover, other studies report that H. hepaticus induces colitis in IL-10–deficient mice (52, 53), highlighting a possible link between TLR5 and IL-10+ macrophages in H. hepaticus pathogenesis. Here, we demonstrate that TLR5 signaling is essential for mucosal protection by promoting the recruitment of CCR2+ cells and the maturation of LP macrophages, which are key producers of IL-10 in the gut, highlighting a possible link between TLR5 and IL-10+ macrophages in H. hepaticus pathogenesis.

Previous work demonstrated that TLR5 expression differs by intestinal region, with expression restricted to Paneth cells in the small intestine crypt but distributed more broadly among colonic epithelial cells (54). Three-dimensional (3D) mouse Paneth cells enriched small intestinal organoids, and colonoids (which contain both undifferentiated and differentiated cells) responded to flagellin and up-regulated chemokines (54); however, the specific flagellin-responsive colonic cell types remained undefined. In addition, early studies using human epithelial cell lines showed that TLR5 localizes to the IEC basolateral surface, suggesting that flagellin sensing is limited to situations where bacterial products cross the epithelial barrier (55, 56). Our current study advances this understanding by using HCMs that allow for functional separation of DF IECs and UD stem-like cells, which express higher TLR5. After apical or basolateral treatment, UD, but not DF, HCMs responded to TLR5 stimulation. Similar to HCMs, in the mouse epithelium, we found higher Tlr5 expression in LGR5+ stem cells than mature LGR5 IECs. These results suggest that colonic stem cells in humans and mice, such as Paneth cells in the small intestine, act as critical sensors of flagellated microbes and highlight a conserved mechanism to spatially restrict microbial recognition to the crypt base to safeguard the stem cell niche. Under homeostatic conditions, stem cells are physically shielded from microbial stimulation by mucus, secretory immunoglobulin A (IgA), and antimicrobial peptides (13). However, multiple studies showed colonization of cecal and colonic crypts with select flagellated commensal bacteria at homeostasis, which could induce TLR5 signaling (4749, 57). Furthermore, disruption of the epithelial barrier during injury and resulting expansion of the stem cell zone may increase stem cell and microbial interactions. We propose that compartmentalized TLR5 signaling provides a protective strategy, which promotes tonic macrophage expansion in the steady state and enables amplification when epithelial integrity is compromised or after colonization with microbes that can reach the base of the crypt.

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