Latest news with #ASOs
Time of India
2 days ago
- Politics
- Time of India
HC directs govt to revise ASO seniority list based on appointment date
1 2 Cuttack: Orissa high court has directed the state govt to revise the seniority list of assistant section officers (ASOs)in the Odisha Secretariat Service, impacting hundreds of employees. The vacation bench's verdict settles a long-standing dispute concerning seniority among two batches of ASOs — direct recruits appointed through two separate advertisements and between promotees and direct recruits. Further, the verdict brings clarity to service-related disputes that lingered for years while providing relief to employees who were appointed earlier but placed lower in the final gradation list of ASOs published on June 11, 2020. A total of 10 writ petitions were clubbed together for hearing, categorised into two groups. The first group, comprising seven petitions, involved a dispute between two sets of direct recruits: one recruited under Odisha Public Service Commission (OPSC)'s advertisement no. 06 dated May 14, 2015, for ST category candidates (140), and another (811) under advertisement no. 08 of Oct 6, 2012. The second group of three petitions involved disputes between promotees and direct recruits. The HC noted that although advertisement no. 6 was issued earlier, appointments from the list were delayed until Oct 2016 due to legal hurdles and administrative delays. In contrast, candidates under the 2015 advertisement were appointed earlier — on Jan 27 and May 18, 2016. In the judgment on June 3, the vacation bench of Justice B P Routray upheld the principle that seniority in govt service should be based on the actual date of appointment, not the date of the recruitment advertisement or recommendation — unless a rule explicitly states otherwise. Justice Routray ruled that ASOs appointed earlier in 2016 under advertisement no. 6 must be placed above those appointed later in the same year under advertisement no. 8 in the final gradation list published on June 11, 2020. Justice Routray further ruled that promotees must be treated as en-bloc seniors to the direct recruits of the same calendar year. Accordingly, Justice Routray ordered the home department to revise the ASO gradation list in line with the HC's directives, ensuring that seniority reflects the actual date of appointment. The judgment reinforced a key service jurisprudence, "He who is appointed earlier, ranks earlier. " Get the latest lifestyle updates on Times of India, along with Eid wishes , messages , and quotes !
New Indian Express
2 days ago
- Politics
- New Indian Express
Orissa HC directs govt to revise gradation list of secretariat ASOs
The bench of Justice AK Mohapatra noted that although Advertisement No. 08 was issued earlier in 2012, appointments from this list were delayed until October 2016 due to legal hurdles and administrative delays. In contrast, candidates under the 2015 advertisement were appointed on January 27, 2016 and May 18, 2016. Justice Mohapatra endorsed the principle that seniority in government service should be based on the actual date of appointment, not the date of the recruitment advertisement or recommendation, unless a rule explicitly states otherwise. While providing relief to candidates who were appointed earlier but placed lower in the seniority list, Justice Mohapatra ruled that the ASOs appointed earlier in 2016 under Advertisement No. 06 must be placed above those appointed later the same year under Advertisement No. 08 in the final gradation list published on June 11, 2020. The judge further ruled that promotees must be treated as en bloc senior to the direct recruits of the same calendar year and directed the Home department to revise the ASO gradation list in line with the court's directives, ensuring that seniority reflects the actual date of appointment. He also ruled that promotees must be treated as en bloc senior to the direct recruits of the same calendar year.
Associated Press
15-05-2025
- Business
- Associated Press
QurAlis Announces Exclusive License on Novel Mechanism for Fragile X Syndrome (FXS) to Enable Development of First Potential Disease-Modifying Therapy
CAMBRIDGE, Mass.--(BUSINESS WIRE)--May 15, 2025-- QurAlis Corporation ('QurAlis'), a clinical-stage biotechnology company driving scientific breakthroughs into powerful precision medicines that have the potential to alter the trajectory of neurodegenerative and neurological diseases, today announced it has entered into an exclusive license agreement with UMass Chan Medical School ('UMass Chan') on a novel RNA-targeted mechanism confirmed to restore functional protein for Fragile X syndrome (FXS). Fragile X syndrome is the leading inherited form of intellectual disability and the most common single genetic cause of autism. It is a genetic condition caused by a mutation of a single gene – Fragile X messenger ribonucleoprotein 1 (FMR1) – on the X chromosome. This mutation of FMR1 causes a range of developmental problems including learning disabilities, behavioral challenges, and cognitive impairment. QurAlis' exclusive license agreement is a result of its 2024 partnership and collaboration with UMass Chan to explore the biology of FXS to determine and confirm relevant targets that could enable antisense oligonucleotide (ASO)-mediated correction for FXS. QurAlis leveraged its deep understanding, knowledge and expertise in developing ASOs as part of the collaboration. QurAlis confirmed the findings from the original publication of the UMass Chan researchers and is advancing FMR1 as a precision medicine target in up to 80 percent of FXS patients. The mis-spliced form of FMR1, designated as FMR1-217, is widely expressed throughout cortical brain areas affected in FXS and can be measured in blood and cerebrospinal fluid. Preliminary data suggest biomarker feasibility to detect mis-splicing of FMR1 in patients with FXS. 'FXS is a devastating neurodevelopmental disorder with no effective disease-modifying therapies available. Our initial partnership with UMass Chan confirmed that FMR1-217 is a validated genetic target for FXS,' said Kasper Roet, Ph.D., chief executive officer and co-founder of QurAlis. 'This groundbreaking discovery of a novel RNA-targeted mechanism to restore functional protein for FXS and the feasibility of a biomarker to detect mis-splicing of FMR1 in FXS patients opens up a completely new type of therapeutic approach through splice correction. We look forward to applying QurAlis' FlexASO® platform and deep knowledge and expertise of ASO splicing targets toward having a candidate nominated for IND-enabling studies in the near future, so that we can bring a potential new precision medicine option to patients.' Joel Richter, Ph.D., the Arthur F. Koskinas Chair in Neuroscience and professor of molecular medicine at UMass Chan, and colleagues Sneha Shah, Ph.D., and Jonathan K. Watts, Ph.D., together with Elizabeth Berry-Kravis, M.D., Ph.D., at Rush University Medical Center, have shown that aberrant alternative splicing, or mis-splicing, of messenger RNA (mRNA) plays a fundamental role in FXS. In a seminal publication by the group, it was revealed that in FXS patients, FMR1 mRNA is still being expressed, but is mis-spliced, comprising a short, truncated alternative mRNA variant called FMR1-217 which results in non-functional FMRP protein expression. Working with patient-derived cells, Dr. Richter's lab and Dr. Berry-Kravis initially demonstrated that ASOs can successfully inhibit the mis-splicing, reduce expression of FMR1-217, rescue proper FMR1 mRNA, and restore FMRP protein expression. 'This is a meaningful step in the process of taking basic biological discoveries and turning them into practical therapies that can benefit patients in the clinic,' said Dr. Richter. 'QurAlis' platform and expertise in neurodegenerative disorders are industry leading and well positioned to address the mis-splicing of FMR1 RNA and restore functional FMRP protein expression. This partnership has not only validated our years-long research but also has resulted in the confirmation of a novel target for FXS, which we hope will lead to much-needed treatment options for FXS patients and their families.' Dr. Berry-Kravis added, 'I am very excited that we will be able to continue development of this potential genetically based disease-modifying FMRP-restoring therapy that is expected to have a major impact on the FXS field and the spectrum of treatment options available to improve function in people with FXS.' An orphan disease, FXS affects approximately 87,000 individuals in the U.S. alone – one in 4,000 men and one in 6,000 women. Though FXS occurs in both genders, males are more frequently affected than females, and generally with greater severity. In addition to intellectual disability, FXS patients endure a wide range of disabling symptoms including severe anxiety, social aversion, hyperactivity and attention deficit, sensory hypersensitivity, aggression, developmental seizures, and others. There are no effective disease-modifying therapies currently available for FXS. ASOs are short, engineered single-stranded DNA/RNA molecules that can selectively bind RNA to regulate its expression in the cell. ASO technology has been leading in the field of protein regulation and has since allowed us to develop treatments for neurodegenerative disease by changing the expression of genes connected to the disease. QurAlis' FlexASO® platform was developed to generate splice-switching ASOs with improved potency, increased therapeutic index and improved bio-distribution. This bespoke platform has the potential to tackle the spectrum of neurodegenerative and neurological diseases. About QurAlis Corporation At QurAlis, we are neuro pioneers on a quest to cure, boldly seeking to translate scientific breakthroughs into powerful precision medicines. We work collaboratively with a relentless pursuit of knowledge, precise attention to craft, and compassion to discover and develop medicines that have the potential to transform the lives of people living with neurodegenerative and neurological diseases. QurAlis is the leader in development of precision therapies for amyotrophic lateral sclerosis (ALS). In addition to ALS, QurAlis is advancing a robust precision medicine pipeline to bring effective disease-modifying therapeutics to patients suffering from severe diseases defined by genetics and clinical biomarkers. For more information, please visit or follow us on X @QurAlisCo or LinkedIn. View source version on CONTACT: Kathy Vincent [email protected] 310-403-8951 KEYWORD: UNITED STATES NORTH AMERICA MASSACHUSETTS INDUSTRY KEYWORD: RESEARCH NEUROLOGY GENETICS BIOTECHNOLOGY HEALTH UNIVERSITY PHARMACEUTICAL SCIENCE EDUCATION SOURCE: QurAlis Corporation Copyright Business Wire 2025. PUB: 05/15/2025 07:45 AM/DISC: 05/15/2025 07:44 AM
Business Wire
15-05-2025
- Business
- Business Wire
QurAlis Announces Exclusive License on Novel Mechanism for Fragile X Syndrome (FXS) to Enable Development of First Potential Disease-Modifying Therapy
CAMBRIDGE, Mass.--(BUSINESS WIRE)-- QurAlis Corporation ('QurAlis'), a clinical-stage biotechnology company driving scientific breakthroughs into powerful precision medicines that have the potential to alter the trajectory of neurodegenerative and neurological diseases, today announced it has entered into an exclusive license agreement with UMass Chan Medical School ('UMass Chan') on a novel RNA-targeted mechanism confirmed to restore functional protein for Fragile X syndrome (FXS). Fragile X syndrome is the leading inherited form of intellectual disability and the most common single genetic cause of autism. It is a genetic condition caused by a mutation of a single gene – Fragile X messenger ribonucleoprotein 1 (FMR1) – on the X chromosome. This mutation of FMR1 causes a range of developmental problems including learning disabilities, behavioral challenges, and cognitive impairment. QurAlis' exclusive license agreement is a result of its 2024 partnership and collaboration with UMass Chan to explore the biology of FXS to determine and confirm relevant targets that could enable antisense oligonucleotide (ASO)-mediated correction for FXS. QurAlis leveraged its deep understanding, knowledge and expertise in developing ASOs as part of the collaboration. QurAlis confirmed the findings from the original publication of the UMass Chan researchers and is advancing FMR1 as a precision medicine target in up to 80 percent of FXS patients. The mis-spliced form of FMR1, designated as FMR1-217, is widely expressed throughout cortical brain areas affected in FXS and can be measured in blood and cerebrospinal fluid. Preliminary data suggest biomarker feasibility to detect mis-splicing of FMR1 in patients with FXS. 'FXS is a devastating neurodevelopmental disorder with no effective disease-modifying therapies available. Our initial partnership with UMass Chan confirmed that FMR1-217 is a validated genetic target for FXS,' said Kasper Roet, Ph.D., chief executive officer and co-founder of QurAlis. 'This groundbreaking discovery of a novel RNA-targeted mechanism to restore functional protein for FXS and the feasibility of a biomarker to detect mis-splicing of FMR1 in FXS patients opens up a completely new type of therapeutic approach through splice correction. We look forward to applying QurAlis' FlexASO® platform and deep knowledge and expertise of ASO splicing targets toward having a candidate nominated for IND-enabling studies in the near future, so that we can bring a potential new precision medicine option to patients.' Joel Richter, Ph.D., the Arthur F. Koskinas Chair in Neuroscience and professor of molecular medicine at UMass Chan, and colleagues Sneha Shah, Ph.D., and Jonathan K. Watts, Ph.D., together with Elizabeth Berry-Kravis, M.D., Ph.D., at Rush University Medical Center, have shown that aberrant alternative splicing, or mis-splicing, of messenger RNA (mRNA) plays a fundamental role in FXS. In a seminal publication by the group, it was revealed that in FXS patients, FMR1 mRNA is still being expressed, but is mis-spliced, comprising a short, truncated alternative mRNA variant called FMR1-217 which results in non-functional FMRP protein expression. Working with patient-derived cells, Dr. Richter's lab and Dr. Berry-Kravis initially demonstrated that ASOs can successfully inhibit the mis-splicing, reduce expression of FMR1-217, rescue proper FMR1 mRNA, and restore FMRP protein expression. 'This is a meaningful step in the process of taking basic biological discoveries and turning them into practical therapies that can benefit patients in the clinic,' said Dr. Richter. 'QurAlis' platform and expertise in neurodegenerative disorders are industry leading and well positioned to address the mis-splicing of FMR1 RNA and restore functional FMRP protein expression. This partnership has not only validated our years-long research but also has resulted in the confirmation of a novel target for FXS, which we hope will lead to much-needed treatment options for FXS patients and their families.' Dr. Berry-Kravis added, 'I am very excited that we will be able to continue development of this potential genetically based disease-modifying FMRP-restoring therapy that is expected to have a major impact on the FXS field and the spectrum of treatment options available to improve function in people with FXS.' An orphan disease, FXS affects approximately 87,000 individuals in the U.S. alone – one in 4,000 men and one in 6,000 women. Though FXS occurs in both genders, males are more frequently affected than females, and generally with greater severity. In addition to intellectual disability, FXS patients endure a wide range of disabling symptoms including severe anxiety, social aversion, hyperactivity and attention deficit, sensory hypersensitivity, aggression, developmental seizures, and others. There are no effective disease-modifying therapies currently available for FXS. ASOs are short, engineered single-stranded DNA/RNA molecules that can selectively bind RNA to regulate its expression in the cell. ASO technology has been leading in the field of protein regulation and has since allowed us to develop treatments for neurodegenerative disease by changing the expression of genes connected to the disease. QurAlis' FlexASO® platform was developed to generate splice-switching ASOs with improved potency, increased therapeutic index and improved bio-distribution. This bespoke platform has the potential to tackle the spectrum of neurodegenerative and neurological diseases. About QurAlis Corporation At QurAlis, we are neuro pioneers on a quest to cure, boldly seeking to translate scientific breakthroughs into powerful precision medicines. We work collaboratively with a relentless pursuit of knowledge, precise attention to craft, and compassion to discover and develop medicines that have the potential to transform the lives of people living with neurodegenerative and neurological diseases. QurAlis is the leader in development of precision therapies for amyotrophic lateral sclerosis (ALS). In addition to ALS, QurAlis is advancing a robust precision medicine pipeline to bring effective disease-modifying therapeutics to patients suffering from severe diseases defined by genetics and clinical biomarkers. For more information, please visit or follow us on X @QurAlisCo or LinkedIn.
Yahoo
12-02-2025
- Health
- Yahoo
New insights on heart disease and menopause
As if hot flashes, mood swings, uncomfortable sex, and a host of other symptoms weren't enough to deal with, menopause is also a time when a woman's risk of cardiovascular disease shoots up to match men her age. Although scientists have known this for some time, new research is beginning to shed light on the complex link between heart disease and menopause, Hone Health reports. One factor is declining estrogen levels during perimenopause, which removes some of the hormone's cardioprotective effects, physician Ella Ishaaya M.D. says. "Estrogen downregulates inflammatory markers, prevents buildup of lipids and LDL, and a number of other things." Once that happens, your body shifts toward a more androgenic profile—meaning it's more like that of a man's—and cardiovascular risks rise. But you don't have to accept these changes. New research has identified screenings and medications that may help detect and address heart disease sooner, potentially leading to better outcomes. Most of us know high levels of triglycerides and LDL (bad) cholesterol are red flags for heart health. Recently, another lesser-known cardiovascular biomarker, lipoprotein (a) or Lp(a), has also been making headlines. Lipoprotein (a) is structurally similar to LDL but has a second protein called apolipoprotein(a) attached to it, cardiologist Anurag Mehta, M.D., explains. "It's associated directly with the [heightened] risk of cardiovascular disease, heart attack, stroke, and a heart valve problem called aortic stenosis," he adds. While Lpa levels remain relatively stable throughout your life, they increase after menopause. It's unclear why, Mehta says. "There's some thought that estrogen levels [regulate] levels of Lp(a)." Genetics also play a role, making it difficult to manage Lp(a) levels through lifestyle changes alone. "The impact of menopause and lifestyle factors like diet and exercise tends to be small," Mehta says. Additionally, "there are well-known race and ethnic differences in Lp(a) levels." Black people generally have levels three times higher than white people, and South Asians twice as high. Fortunately, hormone replacement therapy (HRT)—also called menopause hormone therapy (MHT)—appears to help lower lipoprotein(a). Other emerging therapies may be available in the coming years, including the following medications: Antisense oligonucleotides (ASOs) inhibit the production of apolipoprotein(a) and reduce Lpa by up to 80 percent or more in trials. RNAi are small, interfering RNA molecules that silence the gene that encodes Lp(a). An early-stage clinical trial showed a single dose decreased Lp(a) by up to 98 percent. If further testing confirms the safety and efficacy of these and other medications, FDA approval is anticipated in the next two to three years, Mehta says. Studies will have to show that these drugs can lower Lp(a) and improve cardiovascular outcomes. Getting a lipoprotein(a) screening Although one in five people have high Lp(a) levels, a standard lipid panel doesn't measure this biomarker. European and Canadian guidelines recommend everyone be screened once. But in the U.S., doctors typically only recommend checking your lipoprotein(a) if: You're younger than 65 and have had a heart attack You have a family history of early cardiovascular disease You have high LDL that can't be controlled by statins If you're interested in testing, talk to your healthcare provider about your risk factors. Calcifications in the coronary arteries indicate plaque buildup, or atherosclerosis, which can lead to heart disease. A coronary artery calcium (CAC) test can help assess your risk. It's a CT scan that measures calcium in the arteries supplying blood to the heart, with a higher score indicating a greater risk of heart problems. "Think of the coronary arteries as a plumbing system," physician Ella Ishaaya, M.D. says. "If you develop some gunk in your faucet, the water will still pass." But as the gunk forms and gets larger, it will eventually clog the faucet, and only a little water will pass through. The heart operates similarly. "The coronary arteries supply blood to the heart," Ishaaya says. A build-up of calcium and other inflammatory cells could calcify and become hard plaque. If this plaque ruptures or erodes in the coronary artery, it can cause a blood clot to form, which blocks blood flow to your heart and causes a heart attack. Coronary artery calcification accelerates after menopause, increasing these risks. In a recent study led by Ishaaya, researchers found among patients taking statins, CAC scores increase faster in postmenopausal women compared to men of the same age, showing a median rise of 31 points in a year—roughly double the rate for men. One possible explanation, Ishaaya says, is the decline in cardioprotective estrogen. When to consider a CAC test Though Ishaaya says anyone at risk for heart disease should get a CAC test, your insurance may not cover the CT scan needed to spot it. The American College of Cardiology and American Heart Association guidelines recommend a CAC test for people with an atherosclerotic cardiovascular disease (ASCVD) risk of 7.5 to 20 percent to determine if statins would be recommended. Here's how CAC scores are categorized: 0 = No disease 1-99 = Mild disease 100-399 = Moderate disease 400+ = Severe disease "Anything greater than zero means you have a degree of calcium buildup in your heart, so you should make lifestyle modifications to mitigate that risk," Ishaaya says. "Once your score is in the double digits, we think about statin therapy." However, if you have a family history of atherosclerosis or have multiple risk factors for the condition, statins may be a great preventive measure—regardless of your CAC score. Hot flashes aren't just annoying—they may indicate a higher risk of heart problems. In a study published in the Journal of the American Heart Association in 2021, women whose hot flashes persisted for an average of four annual checkups had a 77 percent increased risk of cardiovascular disease. Researchers aren't sure why, but women with hot flashes often have higher levels of cholesterol, LDL, triglycerides, blood pressure, and insulin resistance than women who don't. Steps to take if you have hot flashes Using hormone replacement therapy (HRT) to reduce cardiovascular risk during menopause remains a topic of debate. The Menopause Society doesn't recommend HRT for heart health alone in women who enter menopause at the average age (around 52), a position supported by several studies. However, some studies suggest estrogen therapy may reduce the risk of heart disease and death in healthy women under 60 who are within 10 years of menopause. Ultimately, "we need more data," gynecologist Brandye Wilson-Manigat, M.D., FACOG, says. "There are so many formulations of estrogen now; the dosings are different, and how you administer the medications is different. All of that may have some impact on the benefits and risks of cardiovascular disease in using them." Deciding whether or not to take HRT—and for how long to take it—should be a conversation between you and your physician. They will take into consideration your age, how long you've been in menopause, your personal and family history of heart health, other medications you're taking, and more. Although you can't avoid menopause, you can take action to prevent cardiovascular disease. "Making lifestyle and diet changes can have a very beneficial effect [on your heart health]," Mehta says, even if you have high Lp(a) levels or a family history. Consider these expert-backed recommendations: Get screened regularly In addition to the biomarkers mentioned above, get your lipid panel checked annually to stay on top of your total cholesterol, LDL, HDL, and triglycerides. Keep in mind: You can have normal cholesterol levels and a high CAC score. Manage other conditions Hypertension, diabetes, obesity, and high cholesterol—alone or combined—increase the risk of heart disease. Mehta recommends working with your medical team to manage these conditions as best you can through lifestyle changes and medication. Stay active Research shows that higher levels of physical activity are linked to a lower risk of cardiovascular disease. Aim for 150 minutes of moderate aerobic exercise or 75 minutes of vigorous aerobic exercise weekly, plus at least two days of strength training per week. Eat a heart-healthy diet The Mediterranean, DASH, and plant-based diets have the most evidence for preventing heart disease. Prioritize minimally processed foods such as vegetables, fruits, legumes, nuts, lean proteins, and healthy fats, including olive oil and avocados. Talk to your doctor about treatment options The best medication for women going through perimenopause is the one that's unique to their symptoms and health history—meaning, it requires a conversation with your doctor. For anyone with elevated LDL cholesterol levels or a high CAC score, statins are typically recommended. "Statin therapy is one of the mainstays of treatment that we have to lower cardiovascular risk," Mehta says. This story was produced by Hone Health and reviewed and distributed by Stacker.
