Yes, social media is making kids depressed
What they found was clear: when social media use increased, so did the children's depressive symptoms.But the opposite wasn't true. Children who were already feeling low or depressed were not more likely to start using social media than others.On average, the amount of time pre-teens spent on social media went from 7 minutes a day to 73 minutes a day over the three years.At the same time, their depressive symptoms, which include feelings of sadness, hopelessness, or lack of interest, rose by 35%.
Mobile phone use increasing depression symptoms in teenagers. ()
Dr. Jason Nagata, the lead author and associate professor of paediatrics at UCSF, explained that this study is one of the first to track the same children over time.advertisement"These findings provide evidence that social media may be contributing to the development of depressive symptoms,' he said.The study didn't explore the exact reasons why social media causes these emotional changes, but past research points to several possibilities. One is cyberbullying, which means being bullied online. Another is disrupted sleep, especially when teenagers stay up late using phones and miss out on rest.Dr. Nagata's team recently published another study showing that kids who are cyberbullied are more than twice as likely to have thoughts of suicide and also more likely to try substances like alcohol, marijuana, or nicotine.Even though social media can cause harm, it also plays a big part in how children today connect with friends and express themselves. That's why experts recommend helping kids use it in healthier ways rather than banning it completely.The American Academy of Pediatrics suggests families create a Family Media Plan: a guide to help kids and parents decide when and how to use screens.Dr. Nagata advises parents to have open conversations and set screen-free times, like during meals or before bedtime, for the whole family.Must Watch
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Business Standard
21 hours ago
- Business Standard
2023's marine heatwaves signal early irreversible coral damage: Study
Marine heatwaves -- prolonged periods of raised ocean temperatures than what are typical for that time of year -- experienced in 2023 were not only unprecedented, but may have also signalled a potential climate tipping point, with irreversible, negative impacts to coral reefs and ecosystems, according to a new study. Researchers from China and the US found that regions in oceans across the globe, including the North Atlantic, and the tropical, south and north Pacific experienced extreme marine heatwaves -- the longest in duration, widest in extent and highest in intensity on record. The findings, published in the journal Science, show that the most intense warming occurred in the North Atlantic, tropical eastern Pacific, north Pacific, and southwest Pacific, which "collectively accounted for 90 per cent of the global ocean warming". Heatwaves in the North Atlantic which began mid-2022 persisted for 525 days with an intensity four times the typical, making it "the longest recorded marine heatwave in the region", the authors said. The southwest Pacific heat event broke records for its expanse and prolonged duration, while unusual temperatures in the tropical eastern Pacific peaked at 1.63 degrees Celsius during the onset of El Nino, they said. 'El Nino' is the warm phase of the 'El Nino-Southern Oscillation' (ENSO) natural climate pattern, which involves changes in temperatures and atmospheric pressures in the Pacific Ocean. El Nino is linked with warmer ocean temperatures. The authors, including those from the US' Scripps Institution of Oceanography at the University of California, said the marine heatwaves of 2023 were "a global event with a 50-year return period, (with a less than two per cent chance of occurrence)". First author Tianyun Dong, a joint postdoctoral researcher at the Eastern Institute of Technology, Ningbo, and Southern University of Science and Technology in China, told PTI in an email, "Global warming, observed over a long-term and primarily driven by greenhouse gas emissions, has raised the ocean's baseline state, making marine heatwaves increasingly frequent and intense." Further, the trends observed also suggest a "possible indication of an approaching climatic tipping point", the study said. A climate tipping point, potentially a 'point of no return', is related with irreversible, disproportionate health and economic consequences for the world's most vulnerable, such as tropical coral reefs, and ice sheets of Greenland and Antarctica. "While a full (ocean-climate) system collapse has not occurred, irreversible impacts -- mass coral bleaching in tropical reefs, collapse of key habitats -- are already emerging," Dong said. Coral bleaching in reefs, or the loss of algae in reefs causing a 'whitening' and vulnerability to disease and death, are showing few signs of recovering, while the functional collapse of key habitats in some of the world's regions undermine biodiversity and the role of ecosystems, Dong explained. "These impacts reflect more than a short-term stress, suggesting a shift towards a permanent ecological change. The 2023 marine heatwaves may, therefore, mark a dangerous step closer to tipping points in the ocean-climate system," the first author said. Arpita Mondal, associate professor at the department of civil engineering and centre for climate studies, IIT Bombay, and not involved with the study, told PTI, "Based on a primary reading of the paper, I'm quite convinced of the scientific robustness." Mondal explained that the ocean and atmosphere "talk to each other through processes -- called the 'teleconnections' -- through which far-away processes can influence local weather". "For example, processes in the southern and equatorial Pacific Ocean can influence the Indian monsoon," she said. "Of course, El Nino is the most significant phenomenon which affects not only monsoons in South Asia, but ENSO-neutral conditions -- where neither El Nino nor La Nina dominate -- have been linked with the heat waves in the pre-monsoon season too," Mondal explained. "Similarly, oscillations and circulation of currents in oceans and atmosphere can impact weather worldwide," she added. The study team analysed satellite observations and temperature data of the world's oceans. Data from the NASA-funded 'ECCO2' project, focussed on producing a high-resolution estimate of the state of the world's oceans and sea ice, was also analysed. First author Dong said that despite a relatively weak El Nino -- studies show its growth rate unexpectedly decelerated in mid-2023 -- the unprecedented nature of 2023's marine heatwaves cannot be explained by natural climate variability alone. "A continued warming of the planet -- especially when combined with El Nino -- could produce even more extreme marine heatwaves, pointing toward a potential new normal of amplified ocean heat extremes and a higher chance of crossing physical and ecological tipping points," the first author said. Mondal, who is not involved in the study, pointed to the concerning lack of reliable, long-term ocean data. "My concern is more about the lack of long-term, reliable ocean data globally. We have only been monitoring oceans in the recent years. We do not have say, 150 to 200 years of ocean surface temperatures recorded. However, satellites developed in the last 50 years or so have definitely helped in complementing the buoys which have been in place for monitoring the ocean," she said.
Time of India
2 days ago
- Time of India
US Scientists discover new early warning sign for deadly pancreatic cancer
With 508,533 new cases and 505,752 deaths worldwide in 2021, pancreatic cancer remains a significant global health challenge with increasing incidence and mortality rates. Pancreatic cancer is often considered deadly due to its tendency to be diagnosed at a late stage, its aggressive nature, and the lack of effective treatments for advanced cases. However, may soon gain a powerful new ally in the battle against this cancer: a biological 'early warning' system that can signal the presence of precancerous pancreatic cells. Researchers at the University of California, San Diego, have uncovered a crucial link between inflammation, cellular stress, and the development of pancreatic ductal adenocarcinoma (PDAC), the most common and aggressive type of pancreatic cancer. What is pancreatic cancer? Pancreatic cancer is a disease in which malignant (cancerous) cells form in the tissues of the pancreas. The pancreas is a gland located behind the stomach that plays a crucial role in digestion and blood sugar regulation by producing enzymes and hormones. While the exact causes are not always clear, risk factors include smoking, family history of pancreatic cancer, long-standing type 2 diabetes, and chronic pancreatitis. Pancreatic cancer is often difficult to diagnose early because symptoms may be subtle or absent in the early stages. The deadliness of PDAC Pancreatic ductal adenocarcinoma (PDAC) originates in the small ducts of the pancreas and carries an incredibly grim prognosis. The average five-year survival rate is less than 10%. According to 2023 estimates, over 62,000 new cases of pancreatic cancer were diagnosed in the US alone. Because it usually shows no symptoms in early stages, PDAC is typically detected only after it has spread, making it hard to treat and nearly impossible to cure. Scientists have long known that inflammation and cellular stress are involved in the growth and spread of pancreatic cancer. But the exact mechanism remained unclear until now. The silver lining In a new study, the UC San Diego team focused on a protein called STAT3 (signal transducer and activator of transcription 3), which is activated under stressful or inflammatory conditions in the body. Once turned on, STAT3 triggers a chain of biological reactions that help tumors grow, adapt, resist treatment, and spread. David Cheresh, a pathologist and co-author of the study, told Newsweek, 'Given the fact that STAT3 plays such an important role in many cancers and the fact that it controls so many genes prompted us to drill down on which genes in particular are associated with cancer development, progression, and drug resistance.' The team also discovered that under low oxygen conditions and inflammation, both common in cancer, STAT3 activates a gene called Integrin β3 (ITGB3) in pancreas cells. This gene speeds up tumor growth and helps cancer spread faster. Even more concerning, they found that common treatments like chemotherapy can also trigger STAT3, which may explain why some tumors become resistant over time. However, the good news is, when researchers blocked STAT3's pathway, they were able to delay the development of tumors, offering a potential new direction for future therapies. The STRESS UP gene signature Through this work, the scientists identified 10 genes, including ITGB3, that STAT3 turns on during stress. Together, they form what the team calls the "STRESS UP" signature, a genetic fingerprint of precancerous activity. As per Cheresh, 'A significant number of patients are what we refer to as 'inducible' for these STRESS UP genes, including ITGB3.' But why is that important? Because it could help doctors predict which patients are likely to develop pancreatic cancer and how aggressive that cancer might become. It could also help determine who is more likely to respond to current treatments. Cheresh added, 'Having knowledge of this gene signature in patients could be valuable since there are known drugs on the market for other diseases that block STAT3 activation and thereby inhibit the expression of the STRESS UP genes in cancer cells.' The importance of early detection (and personalized treatment) The research suggests that STRESS UP could play a role at every stage of pancreatic cancer, from the earliest precancerous lesions to fully drug-resistant tumors and even those that have spread to other organs. According to Cheresh, 'We observed that the STRESS UP gene signature is linked to various critical stages of cancer development including: tumor initiation as precancerous lesions develop into actual tumors, as tumors develop drug resistance, and as tumors develop an invasive or metastatic behavior [when cancer spreads].' The researchers are now examining each of the 10 genes in the STRESS UP signature more closely to develop targeted therapies. One such therapy is already in early clinical trials for patients with drug-resistant cancers. Cheresh explained, 'We are now examining each of these STRESS UP genes for their specific role in the development and progression of cancer with the hope that new specific therapies can be developed. We already have one such therapeutic just now entering clinical trials for patients with drug-resistant cancers.' World Lung Cancer Day 2024: Combating The Deadly Disease With Advanced Treatments
Time of India
2 days ago
- Time of India
Do human lungs make blood? Here's what a popular study says
It is a basic principle in biology- blood is made in the bone marrow. It's where the cells(hematopoietic stem cells (HSCs))responsible for generating red blood cells, white blood cells, and platelets reside. But a striking study from researchers at UC San Francisco (UCSF) is rewriting that narrative. According to new findings published in Blood, the lungs also contain active blood-forming stem cells, capable of producing not only red blood cells but also platelets and key immune cells. The discovery could have direct implications for stem cell therapies and transplant medicine. The UCSF research team, backed by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH), first made this groundbreaking discovery in 2017when they found that mouse lungs were generating up to half of the animal's platelets, a surprising contribution for an organ never thought to be involved in hematopoiesis. These cells, structurally and functionally similar to bone marrow HSCs, weren't merely circulating through the lungs, but seemed to be living in there. To test how capable these cells actually were, scientists isolated HSCs from both lung and bone marrow tissue, grew them in laboratory conditions, and observed what they produced. 'Both types of HSCs thrived in our gold-standard stem cell experiment, but the lung HSC colonies made more red blood cells and megakaryocytes, while the bone marrow colonies tended to make more immune cells,' explained Mark Looney, MD, professor of medicine and laboratory medicine at UCSF and senior author of the study. Rethinking the bone marrow transplant Bone marrow transplants have long been used to treat cancers like leukemia and other blood-related conditions. They involve harvesting stem cells from a donor, often via a blood draw, and using them to rebuild a patient's blood system. But the UCSF team found that nearly 1 in 5 stem cells isolated in bone marrow transplants actually carried markers specific to lung-derived HSCs, suggesting that current stem cell harvests may be drawing from more than just the bone marrow. 'For decades, bone marrow transplants have been a lynchpin in the treatment of cancers like leukemia,' Looney said. 'The lung HSCs could prove to be a second and significant reservoir of these precious stem cells.' The team also demonstrated that human lung HSCs could restore bone marrow function in mice, a powerful indication that these cells aren't just present, they are fully operational. Why would lungs make blood? That question remains unanswered, but there are theories. 'The lungs are critical to blood circulation, so it's tantalizing to see the lung HSCs as an emergency reservoir for red blood cell and platelet production,' said Looney. One possibility is that these cells activate during times of stress or injury, when the body's demand for oxygen-carrying red cells or clot-forming platelets spikes. The lungs, always at the center of the oxygen exchange process, could provide a rapid-response supply.
