Archive for category: News

A new study published in the journal of PloS One found that people who used smartphones while sitting on the toilet had a 46% higher risk of developing hemorrhoids when compared to non-users. One key factor was prolonged toilet time, with 37.3% of phone users reporting spending more than 5 minutes per trip. This research suggest that physicians should ask patients with bowel issues about their smartphone use in the bathroom, as it may be an overlooked contributor to hemorrhoid risk.

This study investigated the link between smartphone use during toilet time and the prevalence of hemorrhoids. The study surveyed 125 adults undergoing screening colonoscopies, provides one of the first multivariate analyses exploring this modern habit. The participants completed detailed surveys about their bathroom behaviors, smartphone usage, and lifestyle factors like fiber intake, physical activity, and frequency of straining. 

Of the 125 participants, 43% were found to have hemorrhoids. Smartphone use on the toilet was common—66% admitted to bringing their devices into the bathroom. Interestingly, smartphone users were younger on average than non-users (mean ages 55.4 vs. 62.1).

The analysis showed that time spent on the toilet was notably longer among smartphone users. While only 7.1 percent of non-users reported sitting for more than 5 minutes per visit, a substantial 37.3% of smartphone users did so. The study pointed out that prolonged sitting can increase rectal pressure, which is a known risk factor for hemorrhoids.

After accounting for potential confounding factors like age, sex, body mass index, fiber intake, straining, and physical activity, this association held. Smartphone use on the toilet was linked to a 46% increased risk of hemorrhoids, a finding that reached statistical significance (p = 0.044).

Beyond the numbers, the study also explored what people actually do on their phones while seated. The most common activity was reading news, reported by 54.3% of users, followed by scrolling through social media (44.4%).

Taken together, the findings suggest that the seemingly harmless habit of checking phones in the bathroom may be contributing to a quiet rise in hemorrhoid cases. While the study does not prove causation, the research found that the data adds weight to long-standing anecdotal advice to limit the time spent sitting on the toilet.

Overall, the study recommend that physicians consider asking about smartphone use when evaluating patients with hemorrhoids and that public health messaging address the potential consequences of prolonged toilet sitting.

Source:

Ramprasad, C., Wu, C., Chang, J., Rangan, V., Iturrino, J., Ballou, S., Singh, P., Lembo, A., Nee, J., & Pasricha, T. (2025). Smartphone use on the toilet and the risk of hemorrhoids. PloS One, 20(9),. https://doi.org/10.1371/journal.pone.0329983

Macular edema (ME) develops when fluid leaks into the macula, the central part of the retina responsible for sharp vision, typically as a result of retinal vascular leakage in conditions such as age-related macular degeneration (AMD), branch retinal vein occlusion (BRVO), or diabetic retinopathy. Vascular endothelial growth factor (VEGF) fuels abnormal vessel growth and leakage, making anti-VEGF injections the gold standard for restoring vision. However, treatment response is inconsistent, and the risk of side effects remains. While genetics and protein studies have offered partial insights, the small molecules that mirror the eye’s functional state-metabolites-have been less explored. Because of these gaps, researchers set out to map in detail the metabolic shifts triggered by anti-VEGF therapy in ME.

In a study published July 14, 2025, in Eye and Vision, scientists from Wenzhou Medical University decoded the “metabolic footprints” left by anti-VEGF therapy in patients with ME. Using high-resolution metabolomics, they examined eye fluid before and after treatment, revealing distinct chemical landscapes for different disease causes. The work offers the first comprehensive map of how vision-saving injections rewire the eye’s molecular machinery-knowledge that could help doctors predict treatment success and tailor care to each patient’s unique disease profile.

The team collected 120 aqueous humor samples from 60 ME patients-20 each with AMD, BRVO, and diabetic macular edema (DME)-before and about a month after anti-VEGF injections. Untargeted LC–MS/MS analysis showed a clear metabolic shift post-treatment, with 84 metabolites upregulated and 61 downregulated. Many changes involved amino acid and carbohydrate metabolism, while others reflected reductions in lipid-related pathways.

The metabolic patterns differed by disease. AMD-ME showed pronounced changes in amino acid metabolism and suppression of the TCA cycle and purine metabolism, both key to retinal energy balance. BRVO-ME displayed marked lipid metabolism suppression, particularly in fatty acid biosynthesis, alongside shifts in glycerophospholipids. DME revealed a complex web of altered amino acid, lipid, and carbohydrate pathways, including increased cysteine–methionine and sphingolipid metabolism. Across all subtypes, glucose levels rose and homocysteine dropped—two metabolites closely tied to blood vessel growth—hinting at shared therapeutic effects. Together, these findings suggest anti-VEGF therapy reshapes the biochemical environment of the eye in ways that are both common and disease-specific.

“Our research shows that anti-VEGF therapy doesn’t just seal leaky vessels—it rewires the eye’s chemistry in ways we’re only beginning to understand,” said Dr. Meng Zhou, senior author of the study. “By identifying the molecular signatures unique to each type of ME, we open the possibility of predicting who will benefit most from treatment. This could mark a step toward more personalized, efficient care, ensuring that every patient gets the right therapy at the right time.”

The findings offer a roadmap for bringing metabolomics into the clinic. By tracking metabolite changes before and after treatment, clinicians could monitor therapeutic response in real time, detect early signs of resistance, and adjust strategies accordingly. Subtype-specific metabolic profiles could guide tailored treatments—for example, targeting lipid metabolism in BRVO or amino acid pathways in AMD. Beyond eye care, the approach exemplifies how mapping biochemical changes can reveal hidden layers of disease biology, ultimately enabling precision medicine. As tools for metabolic analysis become more accessible, such strategies could transform how retinal diseases are diagnosed, treated, and monitored worldwide.

Reference:

Yan, C., Yi, Q., Ge, L. et al. Metabolomics analysis uncovers metabolic changes and remodeling of anti-VEGF therapy on macular edema. Eye and Vis 12, 28 (2025). https://doi.org/10.1186/s40662-025-00444-2

Prostate cancer remains a global health challenge, ranking as the second most common malignancy among men. While early-stage disease can be effectively managed, advanced forms-particularly metastatic castration-resistant prostate cancer (mCRPC)-pose significant therapeutic hurdles. A growing body of evidence highlights the pivotal role of SOX transcription factors, with SOX2 emerging as a central driver in tumor growth, spread, and resistance to therapy.

SOX2 is intricately linked to the fate of cancer stem/progenitor cells, influencing processes such as cell proliferation, apoptosis resistance, and epithelial-mesenchymal transition (EMT), which fuel invasion and metastasis. Elevated SOX2 levels are frequently observed in aggressive tumors and are associated with poor prognosis. Its activity extends to shaping tumor lineage plasticity, enabling cancer cells to adapt and survive under therapeutic pressure. This adaptability often facilitates transformation into neuroendocrine prostate cancer (NEPC), an aggressive variant with limited treatment options.

At the molecular level, SOX2 operates within a complex regulatory network, interacting with key transcription factors, non-coding RNAs, and epigenetic modifications. It is also a critical node in multiple signaling pathways, including PI3K/AKT, Hedgehog, Wnt/β-catenin, and TGF-β, which collectively sustain cancer stem cell traits and drive disease progression. Importantly, SOX2’s regulation involves both upstream inducers such as BRN2, TRIB2, and NRP2, and downstream effectors including LSD1, H19, SPINK1, and ASCL1—each contributing to tumor aggressiveness and therapeutic resistance.

SOX2’s role in treatment resistance is particularly significant. It supports resistance to chemotherapy by inducing a reversible quiescent state and activating survival pathways, while also mediating resistance to nuclear hormone receptor signaling inhibitors through modulation of cell cycle regulators and glucocorticoid receptor expression. This makes SOX2 a critical obstacle in sustaining long-term therapeutic success in advanced prostate cancer.

The potential of targeting SOX2-directly or indirectly-offers a promising avenue for innovation. Strategies may include disrupting its protein-protein interactions, modulating upstream regulators or downstream pathways, and harnessing small-molecule inhibitors to selectively curb its tumor-promoting functions. However, given SOX2’s importance in normal tissue regeneration, therapeutic approaches must balance efficacy with safety to minimize adverse effects.

As research advances, understanding the multifaceted role of SOX2 could pave the way for more precise, effective, and durable treatments, offering hope for patients battling the most aggressive forms of prostate cancer.

Reference:

Guotu Du, Xiang Huang, Peng Su, Ying Yang, Shicheng Chen, Tianyu Huang, Neng Zhang, The role of SOX transcription factors in prostate cancer: Focusing on SOX2, Genes & Diseases, https://doi.org/10.1016/j.gendis.2025.101692.