DAILY NEWS BULLETIN LEADING HEALTH, POPULATION AND FAMILY WELFARE STORIES OF THE Day Thursday

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1 DAILY NEWS BULLETIN LEADING HEALTH, POPULATION AND FAMILY WELFARE STORIES OF THE Day Thursday Pollution Delhi Pollution dipped this winter, but only just, reveals data (The Indian Express: ) The improvement has been attributed to the action taken on the ground to control pollution. EPCA also decided to lift the very poor to severe air quality restriction under the Graded Response Action Plan for Delhi-NCR. 15 days, 70 teams: Delhi and Centre tie up for cleaner air15 days, 70 teams: Delhi and Centre tie up for cleaner air Union Budget 2018: To end stubble-burning and fight pollution, a scheme for farmersunion Budget 2018: To end stubble-burning and fight pollution, a scheme for farmers Delhi pollution: Scheme to support ways to manage crop residue, but Budget smokey on allocationdelhi pollution: Scheme to support ways to manage crop residue, but Budget smokey on allocation Delhi saw lower pollution peaks this winter as compared to the last, despite the overall temperatures and wind speed remaining the same as last winter, stated an analysis by the Supreme Court-mandated Environment Pollution (Prevention and Control) Control Authority (EPCA) and the Centre for Science and Environment (CSE). The difference in pollution peaks, however, was not very high. The PM 2.5 peak in 2016 was 759 micrograms per cubic metre 12.7 times more than the standard of 60 micrograms per

2 cubic metre. The peak in 2017 was 686 micrograms per cubic metre 11.4 times higher than the standard. The improvement has been attributed to the action taken on the ground to control pollution. EPCA also decided to lift the very poor to severe air quality restriction under the Graded Response Action Plan for Delhi-NCR. This means that the use of diesel generator is no more restricted and the Badarpur Power plant, which has been shut for four months, can begin functioning again on March 1. However, very little difference in pollution levels was seen in industrial areas, the report states. EPCA chairperson, Bhure Lal, said that for 2018, one of the main focus points was to regulate illegal industries. Stopping illegal industries from operating is going to be a big task this year, he said. Delhi government s power department officials said, Badarpur station can be closed permanently once the 400 kv sub station at Tughlakabad is built. Officials expect this to happen soon and said they are confident that the plant can be shut by the July 2018 deadline. Heart Disease Larger waist, hips may raise women's heart attack risk (Medical News Today: ) It is known that obesity raises the risk of heart attack in both men and women, but recent research published in the Journal of the American Heart Association finds that for women, the size of their hips and waist may be the best indicators of risk. For women, their waist size and waist-to-hip ratio may have an impact on heart attack risk, according to a new study. A higher body mass index (BMI) is known to raise the risk of myocardial infarction, or heart attack, and by and large, this association seems to be the same for both men and women. But as a measurement, BMI says nothing about body fat distribution and does not differentiate between fat types such as visceral fat versus subcutaneous fat.

3 Visceral fat is so named because it builds around one's internal organs, such as the pancreas, liver, and intestines. This type of fat is more closely linked with insulin resistance and other cardiometabolic risk factors. Sex may influence the type of fat that a person is more predisposed to. Studies have revealed, for instance, that men are more likely to accumulate visceral fat, whereas women tend to have more subcutaneous fat. Now, a new study zooms in on body fat distribution and the risk of heart attack. Researchers led by Sanne Peters of the George Institute for Global Health at the University of Oxford in the United Kingdom studied the body size and shape of almost half a million adults to locate the best predictors of heart attack risk. Waist-to-hip ratio dangerous for women Using the U.K. Biobank database, Peters and colleagues examined almost 500,000 people aged between 40 and 69, who were followed up for a period of 7 years. During this time, 5,710 cases of heart attack were recorded 28 percent of which occurred in women. The team applied Cox regression models to calculate the risk of myocardial infarction associated with BMI, as well as "waist circumference, waist-to-hip ratio, and waist-to-height ratio." Waist-to-hip ratio: How does it affect your health? Everything you need to know about your waist-to-hip ratio. The study yielded some interesting results regarding sex differences in heart attack risk. The study authors summarize their findings. "Although general and central adiposity measures each have profound deleterious effects on the risk of [heart attack] in both sexes, a higher waist circumference and waist-to-hip ratio conferred a greater excess risk of [heart attack] in women than in men." "Waist-to-hip ratio was more strongly associated with the risk of [heart attack] than body mass index in both sexes, especially in women," they continue. "Our findings support the notion that having proportionally more fat around the abdomen (a characteristic of the apple shape) appears to be more hazardous than more visceral fat which is generally stored around the hips (i.e., the pear shape)." Sanne Peters However, this is not the first study to draw attention to body fat distribution as being particularly detrimental to women's cardiometabolic health. Previous research that Medical News Today reported on found that, while both men and women had visceral fat, this entailed a higher cardiometabolic risk for women.

4 According to the most recent statistics from the Centers for Disease Control and Prevention (CDC), over 36 percent of adults in the United State are obese, with women being more affected than men. As the CDC note, over 38 percent of U.S. women are obese, while slightly over 34 percent of men have the condition. Parkinson's disease Parkinson's disease: Why do brain cells die? (Medical News Today: ) Researchers have discovered that a molecule already known to be important for other cell functions may also serve as a target against Lewy bodies, which are the toxic protein deposits that build up in the brain in Parkinson's disease. Understanding why brain cells die is key for treating Parkinson's. The molecule, called cardiolipin, is an essential membrane component of mitochondria, which are the tiny powerhouses inside cells that give them energy and help drive their metabolism. Lewy bodies are one hallmark of Parkinson's disease. They contain toxic clusters of alphasynuclein and other proteins that have not folded properly. In a paper now published in the Nature Communications, researchers from the University of Guelph in Canada describe how they discovered "a novel mechanism" in which cardiolipin folds alpha-synuclein. They also found that cardiolipin "can pull" alpha-synuclein out of the toxic clusters and refold it, "thus effectively buffering," or delaying, the progress of the protein's toxicity. "Identifying the crucial role cardiolipin plays," notes senior study author Scott D. Ryan, who is a professor from the university's Department of Molecular and Cellular Biology, "in keeping [alpha-synuclein] functional means cardiolipin may represent a new target for development of therapies against Parkinson's disease." Alpha-synuclein mechanism is unclear

5 Parkinson's disease is a brain-wasting disorder that gets worse over time. The condition's most common symptoms include tremors, muscle rigidity, impaired balance and coordination, and slowness of movement. It also has symptoms not related to movement, which include but are not limited to anxiety, depression, sleep disturbance, constipation, and fatigue. Could your tears help to diagnose Parkinson's? Learn how checking alpha-synuclein levels in tear samples might serve as a noninvasive early test for Parkinson's disease. There are more than 10 million people living with Parkinson's worldwide, including around 1 million in the United States and 100,000 in Canada. The disease mostly strikes after the age of 50, although in 10 percent of cases, it can arise earlier. The main difference between Parkinson's disease and other movement disorders is that the former is caused by the death of dopamine-producing cells in the substantia nigra region of the brain. Dopamine is a messenger molecule, or neurotransmitter, that helps to control movement. Many treatments for Parkinson's aim to raise brain levels of dopamine. Although incorrectly folded alpha-synuclein is a feature of Lewy bodies whose presence precede the death of dopamine cells in Parkinson's disease the specific mechanism is somewhat unclear. However, what we do know is that it in its normal form, alpha-synuclein seems to be important for healthy functioning in cells. For instance, there is evidence to suggest that alpha-synuclein is important for neurotransmitter storage and recycling, and it may also have a role in the control of enzymes that raise levels of dopamine. Cardiolipin's effect reduced in brain cells In order to find out how brain cells deal with incorrectly folded alpha-synuclein, Prof. Ryan and his colleagues carried out experiments using human stem cells. "We thought," says Prof. Ryan, "if we can better understand how cells normally fold alphasynuclein, we may be able to exploit that process to dissolve these aggregates and slow the spread of the disease." The researchers compared normal stem cells with those from people with Parkinson's disease who carried a mutated version of the alpha-synuclein gene.

6 Through these experiments, the team discovered that alpha-synuclein attaches to mitochondria inside brain cells, and that the cardiolipin in the mitochondria refolds the protein into non-toxic forms, thus delaying the process of alpha-synuclein toxicity. The scientists also found that the "buffering capacity is reduced" in cells that had the mutated forms of alpha-synuclein that lead to familial Parkinson's disease. Thus, the researchers suggest that the ability of cardiolipin to slow or halt the progress of alpha-synuclein toxicity is eventually overwhelmed and leads to the death of cells in people with Parkinson's disease. They believe that their results could lead to a new drug that slows the progression of the disease by targeting cardiolipin's role in the folding of alpha-synuclein. "The hope is," says Prof. Ryan, "that we will be able to rescue locomotor deficits in an animal model. It's a big step towards treating the cause of this disease." "Based on this finding, we now have a better understanding of why nerve cells die in Parkinson's disease and how we might be able to intervene." Cancer Smoldering multiple myeloma and cancer: What to know (Medical News Today: ) Overview Types SMM vs. MGUS Treatment Progression Complications Outlook Smoldering multiple myeloma is a rare disorder that can lead to a cancer called multiple myeloma. Typically, smoldering multiple myeloma (SMM) has no symptoms, which can make it difficult to detect. There is only one type of SMM. The disorder has different stages depending on how far it has progressed. We explore stages, treatment, and progression of this disorder. What is smoldering multiple myeloma? Blood in a test tube which may reveal smoldering multiple myeloma

7 SMM is often spotted during unrelated blood or urine tests. SMM is caused by unhealthy plasma cells. Plasma cells are part of the immune system that fights off disease. Plasma cells form in the bone marrow, which is the spongy tissue within the bones. When a person has SMM, their body makes too many plasma cells. These cells are abnormal and create unhealthy antibodies called M proteins. Usually, antibodies recognize bacteria and viruses that cause disease and stop them from harming the body. However, M proteins do not work like normal antibodies, as they do not fight disease. Instead, M proteins build up in the bone marrow and can cause problems if they reach a certain level. In most cases of SMM, however, there are not enough M proteins in the body to cause damage. SMM does not usually have any symptoms, so it may go undiagnosed; however, it may be spotted during blood or urine tests that are being carried out for a separate medical issue. Rarely, SMM can develop into a type of cancer called multiple myeloma. SMM makes up around 5 percent of all cases of multiple myeloma and is not considered an active form of the disease. Types Although there is only one type of SMM, it has three different stages: Stage 1: A certain level of unhealthy cells exist, but they are not increasing in number. Stage 2: Myeloma that is progressing slowly without causing damage to the body. Stage 3: Myeloma that is progressing moderately without causing noticeable damage. If a person is diagnosed with SMM, they will be closely monitored to check which stage the disorder has reached. SMM vs. MGUS MGUS (EM-gus) stands for monoclonal gammopathy of undetermined significance. MGUS is a stage before SMM and the disorder also creates too many unhealthy plasma cells and M proteins (though less than in SMM). Although MGUS results in higher levels of these cells in the bone marrow, they do not usually cause any symptoms or any damage to a person's blood, bones, or kidneys. Around 1 percent of people with MGUS will develop multiple myeloma, lymphoma, or amyloidosis per year. Lymphoma refers to a group of blood cancers. Amyloidosis is a group of rare conditions that stop organs and tissues in the body from working properly. Treatment

8 medical checkup Regular medical checkups are recommended to ensure that SMM is not progressing. SMM and MGUS do not usually cause damage to the body. For this reason, a person who has one of these disorders will not usually require treatment. However, a person with SMM will need to have regular medical checkups to ensure the disorder is not progressing or becoming cancerous. The schedule of appointments will usually be as follows: a follow-up appointment 2 to 3 months after SMM is diagnosed if the results of tests are normal, appointments every 4 to 6 months for 1 year if the results of tests are normal after 1 year, appointments every 6 to 12 months Treatment will be given if SMM progresses to multiple myeloma. Treatment will usually include chemotherapy drugs and pain medication but may also include a stem cell transplant. Research is ongoing into the relationship between SMM and multiple myeloma. Part of this research involves clinical trials, which are often carried out to test new medications and treatments. A person with SMM may wish to take part in a clinical trial. They can discuss this with a doctor to find out more about possible risks and benefits, as well as whether there are trials available in their area. Progression Around 10 percent of people with SMM will develop multiple myeloma in the 5 years after diagnosis. After 5 years, the risk of developing multiple myeloma drops to 3 percent per year. Abnormal plasma cells can create tumors in tissue or bone. If one tumor forms, the disease is known as a plasmacytoma. More than one tumor is called multiple myeloma. Tumors can cause weakened bones, damage the kidneys, and lead to high levels of calcium in the blood. Symptoms include bone pain, anemia, numbness, and a higher risk of infection or illness. Complications MGUS and SMM do not usually have any symptoms, but they can sometimes lead to health problems. Levels of M protein in the body can cause tingling or numbness in the hands or feet. The medical term for this feeling is peripheral neuropathy.

9 MGUS and SMM can weaken the bones, which means that people who have these disorders are at greater risk of developing osteoporosis. Osteoporosis is a condition that causes bones to become less dense and more fragile. Weak bones are more likely to break or fracture. People with MGUS and SMM are more than twice as likely to get an infection than the rest of the population. This is because their immune system is weaker, which means their body produces fewer healthy antibodies that can fight disease. To prevent getting an infection, anyone with SMM or MGUS should consider avoiding friends and relatives who have a contagious illness, such as the flu. Washing hands and having a flu vaccination can also help protect against disease. What's to know about multiple myeloma? Multiple myeloma is a cancer of the blood plasma. Learn more about the symptoms and treatment here. SMM is not a cancer. The risk of the disorder becoming multiple myeloma is relatively low, but it should be closely monitored. As SMM does not have any symptoms, many people do not realize that they have it. If a person is diagnosed with SMM, they will be offered regular medical appointments to monitor the stage and progression of the disorder. Cancer (The Asian Age: )

10 Schizophrenia (The Asian Age: )

11 Epilepsy (The Asian Age: ) Urine Test (The Asian Age: )

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13 Dementia Largest study of its kind finds alcohol use biggest risk factor for dementia (Science Daily: ) Centre for Addiction and Mental Health Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study of over one million adults diagnosed with dementia in France. Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study, published in The Lancet Public Health journal, of over one million adults diagnosed with dementia in France. This study looked specifically at the effect of alcohol use disorders, and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol. Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking. The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men (4-5 Canadian standard drinks) and 40 grams (about 3 standard drinks) per day for women. As a result of the strong association found in this study, the authors suggest that screening, brief interventions for heavy drinking, and treatment for alcohol use disorders should be implemented to reduce the alcohol-attributable burden of dementia. "The findings indicate that heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths," says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm. "Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths." Dr. Rehm points out that on average, alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death for these people.

14 For early-onset dementia, there was a significant gender split. While the overall majority of dementia patients were women, almost two-thirds of all early-onset dementia patients (64.9%) were men. Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia. "As a geriatric psychiatrist, I frequently see the effects of alcohol use disorder on dementia, when unfortunately alcohol treatment interventions may be too late to improve cognition," says CAMH Vice-President of Research Dr. Bruce Pollock. "Screening for and reduction of problem drinking, and treatment for alcohol use disorders need to start much earlier in primary care." The authors also noted that only the most severe cases of alcohol use disorder -- ones involving hospitalization -- were included in the study. This could mean that, because of ongoing stigma regarding the reporting of alcohol-use disorders, the association between chronic heavy drinking and dementia may be even stronger. Diabetes New strategy against vascular disease in diabetes (Science Daily: ) An insulin-mimicking peptide not only lowers blood sugars, but also slows the progression of atherosclerosis in mice A peptide called S597, given to mice with metabolic syndrome, reduced their high blood sugar levels and slowed the growth of lesions in their blood vessel walls. It appears to do so by keeping the production of inflammatory white cells in check. The finding suggest a new approach to explore in research to reduce the high risk of heart attack and stroke in people with diabetes. Recent findings suggest a novel approach for protecting people with diabetes from their higher risk of advanced blood vessel disease, which sets the stage for early heart attacks and strokes. Cardiovascular problems from atherosclerosis -- plaque-like lesions forming in artery walls -are the major cause of death in people with type 2 diabetes and metabolic syndrome.

15 People with metabolic syndrome exceed the normal range for several clinical measurements: blood pressure, blood sugar levels, harmful lipids, body mass index, and belly fat. The researchers studied mice with metabolic syndrome. The mice were obese and had impaired glucose tolerance, a sign of pre-diabetes. In the study, an insulin-mimicking synthetic peptide called S597 was shown to both reduce blood sugar levels and slow the progression of atherosclerotic lesions. Insulin, even when it controls diabetes, does not prevent atherosclerosis. The findings are published in the Feb. 26 issue of Diabetes, a peer-reviewed scientific journal of the American Diabetes Association. The senior author is Karin E. Bornfeldt, University of Washington School of Medicine professor of medicine, Division of Metabolism, Endocrinology and Nutrition. Jenny Kanter, UW research assistant professor of medicine, was the lead author. They are scientists at the UW Medicine Diabetes Institute. The study was conducted as a research collaboration with Novo Nordisk A/S. Although S597 is composed of a single chain of amino acids and looks nothing like insulin, S597 can still activate insulin receptors. But, unlike insulin, it's more selective in what it turns on inside the cells. This study showed that, when S597 binds to insulin receptors, it preferentially activated a signaling arm known as the Akt arm, which is associated with lowering blood sugar levels and with other beneficial effects. It only weakly activated, or may have even prevented the activation of, another signaling arm, called the Erk arm, that is suspected of causing undesirable side effects. The researchers were impressed by the mechanisms behind the S597 slow-down of atherosclerotic lesions. Atherosclerosis starts with fatty streaks appearing in blood vessel walls. As the atherosclerotic lesion grows, inflammation provoked by obesity and recruitment of immune cells can speed the growth of the plaque. Certain white blood cells, particularly monocytes that participate in inflammation, and macrophages, or "big eaters" that are supposedly the bloodstream's cleanup crew, are among the culprits. They can become overladen by engulfing lipids, and can turn into foam cells. These cells gather, and then perish. The core of the lesion fills with dead cells and other debris. If it ruptures, a clot can rapidly form in the vessels of the heart or brain. In mice given S597, the problem with excessive white cells in the lesion seems to be nipped at its source: the early stages of production of inflammatory monocytes and macrophages. The S597 treated mice did not seem prone to the high white cell count characteristic of the inflammation induced by metabolic syndrome and obesity.

16 In fact, the amount of blood-forming stem cells in the bone marrow was lowered to levels observed in lean, healthy mice. These stem cells exhibited less activity from the undesirable signaling pathway originating in the insulin receptors. The numbers of macrophages dying in the lesion were also fewer. While the number of intact cleanup cells rose, the relative content of macrophages in the lesion cores did not go up. The S597 may have either kept more macrophages alive longer or impeded their pile up. Probably because of all this influence on white cells, the lesions did not grow with the rapidity expected in diabetes and metabolic syndrome. The researchers also saw that lesions with debris-filled cores were less common in these mice. The researchers noted that the S597 did not alter cholesterol levels in the plasma or systemic inflammation overall. "Cholesterol lowering drugs like statins are making a big impact in our ability to prevent cardiovascular disease associated with metabolic syndrome and diabetes," Bornfeldt said. "We think that the results of this new study provide a conceptually novel treatment strategy to explore as an additional possibility for protecting against advanced atherosclerosis associated with metabolic syndrome and type 2 diabetes." There is only one previous study of the effects of S597 in living organisms. This new study is believed to be the first reported to evaluate the effects of S597 on the blood vessel system. Funding for this work came in part from National Institutes of Health grants and from a STAR postdoctoral fellowship from Novo Nordisk. Three researchers on the study are employed by Novo Nordisk A/S, which also supplied the S597 peptide for testing.

17 Bone Health (Hindustan: )

18 Pregnancy (Hindustan: )

19 Obesity (Hindustan: )

20 è ȡèØ स व ए आम आदम ȧस हत स ȡ (Dainik Jagran: ) तम म ȶ ɉ Ʌयह स मन आय ह न क वल दव ओ ǔã ȣ ɉक न म पर भ ȣ ɉक ल ट ज त ह द श Ʌ जतन त ज स ȡक प श क å ȡ ȡ ȣ ह आ ह, उस द खत ह ए दव ओ तथ इल ज क ȡ ɉक ` Û बन न ȧ Ǿ ह यह इस द खत ह ए भ ह अब तक आम आदम क ब हतर è ȡèØ स व ए ` Þ ȣȳकर ई ज ȧ ɇ@ ȡ Ȣऔर ` Û è ȡèØ स व ए सबक ȡ ȣȳ ɇ@इसस Ï ȡ ȡग भ र स कट इस ȯğ Ʌ ȡ ȣ ȡȲ ȣऔर अर जकत क र कन क f Ȳğ क अभ व ह जसक समय रहत सम ध न Ǔ ȡ ȡह ग Ǔ Ȣ\ è ȡ ɉ ȧमनम न \ ȯ क म र Ȳ 1हम र द श Ʌ जतन त ज स ȡ क प श क å ȡ ȡ ȣ ह आ ह, उस द खत ह ए दव और इल ज क ȡ ɉक ` Û बन न ȧ Ǿ ह यह Ǿ इस द खत ह ए भ ह अब तक आम आदम क ब हतर è ȡèØ स व ए ` Þ ȣȳकर ई ज ȧ ɇ@भल ȣसरक र अब ] ç Ǖ ȡ भव: य जन क तहत ȣ ɉक स हत क ब म मह य कर न ȧ Ǒ ȡ Ʌबढ़ ȣह, इसक ब वज द è Ȣऔर ` Û è ȡèØ स व ए सबक ȡ ȣȳ ɇ@अभ भ Ï ȡ ȡग भ र स कट इस ȯğ Ʌ ȡ ȣ ȡȲ ȣऔर अर जकत क र कन क f Ȳğ क अभ व भ रह ह इसक एक बड़ म मल È ड ज Ȩà Ȣ ȯ दव ओ क ã ȯस ǒ ȯप य ज न ह, जन पर सरक र न [2016 Ʌब न लग य थ अब एक ब र ^Û Ʌब ज र स ब हर क ȡè ȡǑ ȡ ȯ ȧकव यद ǾǕ ह ई ह, È ɉ इधर ĤǕ Ȣ Ȫ [क आद श पर द श क Ĝ ȲĚȪ जनरल न ^ ȧज च क f एक ȯ ȣ Ǒ कर ȣह यह द खत ह ए द स ल पहल जन ȣ 350 दव ओ क ĤǓ Ȳ ȡ गय थ, उनक द श क Ȳ Ǒ दव ȯğ Ʌक ल क र ब र ȣ 4 हज र कर ड़ ǽ ȯक ह, यह एक बड़ म मल बनत ह 1 [2016 Ʌर क क ȡ कई न म Ȳ Ǔ ȡȲ ǕĤ Ȣ Ȫ [ ȣगई थ और अद लत न ब न क गलत ठहर य थ, ȯ प य गय ǓǕ ȡक कई दस र ȯ ɉ Ʌ^Û Ʌब चन ȧ इज जत ȣȳह \ ȯǐ ȡ, ज प न, ĥ ȡȲ, [ Ȣऔर ǒħ ȯ क स थ ȣकई ȯ ɉ Ʌय दव ए ब च ȣȳ

21 ज सकत, ȯ भ रत और क छ \ Û ȡ Ȣ ȯ ɉ क क न न इनक çǖĥ ȡ ɉक ज नत ह ए भ ȡ ȡ[ Ȳ Ǔ ɉक दब व क क रण ^Û Ʌर क ȣȳप रह ɇ@य असल Ʌव स दव ए ɇ, ǔ Û Ʌएक स Ï ȡ ȡ दव ओ क म ल स बन य ज त ह उद हरण क f, Ȱ ȡ ȡ Ȩ और f ǔèĥ द अलगअलग दव ए ɇ, पर Ǒ ^Û Ʌ ȡ क ई नई दव बन ई ज त ह, त वह È ड ज Ȩà Ȣ ȯ कहल त ह 1 [2016 Ʌजब è ȡèØ Ȳğ न तम म कफ स रप सम त ȣ 350 दव ओ क स हत क f ȡǓ ȡ बत य थ त लग थ कम स कम सरक र क उस आम आदम ȧस हत ȧ Đ ह ज [ ȡ ɉक ज ल Ʌफ सकर ȯ è ȧदक न स ǒ ȡ ȨÈ ȣ ȶक ȯ ȡ ȣक ई दव उठ ल त ह और कई ब र [क ल इल ज ह ज न तक उसक स वन करत रहत ह हम र द श Ʌ ɉतक ऐस दव ए ǒ ȡ Ȣब ध क ǒ Ȣ ȣ ɇ@र क लग न क स थ è ȡèØ Ȳğ न ȣ ȣथ Į दव ओ क Ǖè ȯय Èè -ड ज Ȩà Ȣ ȯ (एफड स ) स त य र ह न ȡ ȣ य ज व ण र ध (f Ȳ ȣ ȡ ȪǑ ) और ए टअजय प व र1 ȡçĚȣ k Ǘã Ǔ ȡ[ Ĥ ȡ (एनप प ए) ɮ ȡ ȡ ȡ ȣएक ǐ Ȫ [स अब यह è ç ह ज त ह जनस व क इस ȡ [ पर भ å ȡ ȡǓ ȡ ȡ ȡ ɉ न अपन नजर जम रख ह ǐ Ȫ [ क Ǖ ȡǒ Ǔ Ȣ \ è ȡ न [ ȡ ȣǔ Ȳğ स ब हर ȧदव ओ क Ĥ Ȫ करक ȣ ɉक ब वक फ बन रह ɇ, ǔã è ȡ ɉ और ǐ Ȳ तक क [ बह त बढ़ -चढ़ कर वस ल ज रह ह अपन ज च Ʌ Ĥ ȡ न प य एक म मल Ʌ\ è ȡ न ȣ 13 ǽ ȯक एक ȣ ȯ ȧ ȧ लगभग 190 ǽ ȯ Ǘ ȣह Ǖƨ ल भ लगभग 1000 ȧ स ल कर Ȣख स Ĥ ȡ ȧदव पर 1700 ȧ तक ह Ǖ ȡ ȡ Ȫ ȣ ȧइसस भय कर ȡ द न श यद ȣ Ǖ ह प ए 1Ǔ Ȣ\ è ȡ एक और ȧ क ǐ ȯयह क म कर रह ɇऔर यह ह नई दव ए ईज द करन एनप प ए क म नन ह Ǔ Ȣ\ è ȡ Ȳ Ǔ ɉक स थ स ठग ठ करक ऐस नई दव ए य Ĝ Ȩ Ǿ ȯ ȯ ɇज ȡ ȣ Ǔ Ȳğ स ब हर ह तथ ^Û Ʌबन न ȡ ȣ Ȳ Ǔ ȡȲभ इन दव ओ पर ĤǓ [10 ȧ तक Ǘã Ǚƨ क आन द उठत ɇ@ \ यह प र म मल एक 7 [ ȧ Í Ȣ] ɮ ȡ Ȳ ȧएक Ǔ Ȣ\ è ȡ Ʌह ई Ǚ Ǖक ब द Ĥ ȡ Ʌआय थ जब उसक ǐ ɉक \ è ȡ न 18 ल ख क ǒ थम Ǒ ȡ ǔ Ʌ2700 è ȡ ɉ और 660 ǐ Ȳ क [ भ ȡ थ जसक ब द सरक र ɮ ȡ ȡ^ ȧज च क आद श Ǒ f गए 1Ĥȡ न ȡ ȡȲ ǐ Ȫ [ Ʌसभ Ø ] Ȳ ɉक स थ द श क स मन प श f ɇ, ȯ Ǖ ȡ[Ê स वह \ è ȡ ɉ क ȡ उन दव ओ क \ Ǘã क f क ई ȡ [ ȡ_ ȣȳकर सकत ज सरक र ȧ Ǘã Ǔ Ȳğ स च स ब हर ɇ@ एनप प ए न प य Ǔ Ȣ \ è ȡ ɉ क ǒ क 25 ȧ Ǒ è ȡ ग र Ǔ Ȳǒğ Ǔ ɉ क ह त ह ज स Ȣ ȡ ȣ ȧ ज च, ȸ f ज न ȧ\ ] इस Ǒ è ȯक फ यद उठ कर \ è ȡ ज च स व ओ क न म पर ऊल-ज ल ल प स ऐ ठ ल त ɇ@ ȣस व ए \ Û Ʌġɉपर ȣȳ

22 कम द म पर ` Þ रहत ɇ@ǔ Ȣ \ è ȡ ɉ ȧ Ȩǒ Ȳ मजब त ह न क क रण ȣएक å ȡ ȡ ȣ ȢǓ पहल Ʌ\ Ʌआ ȣ ɇ, ȯ अब È आ चक ह सरक र इनक ȡ ȡ [ ȡ_ कर हर [क छ दव ओ क Ǔ Ȳǒğ Į ȯ Ȣ Ʌअ दर-ब हर f ज न ȡğ स è ȡहल ȣȳ ह सकत \ è ȡ सरक र क Ȱ ɉ स द कदम आग रहत ह ए अपन ग र Ǔ Ȳǒğ दव ओ क ] ɮ रख ह ए ɇ@ Ǒ म जद समय म क ई ȢǓ प श ȡ ज न स भव ȣȳह त Ǔ Ȳǒğ दव ओ ȧस च ȧहर त न म ह ब द Ȣ ȡ ȧज न ȡǑ Ȣ\ è ȡ ɉɮ ȡ ȡइस Ĥ ȡ क å ȡ क एक क रण द श क लचर è ȡèØ Ȳğ भ ह पर f à ȡ ȣ Ǖ ȡक न म पर ȡçĚȣ è ȧ ȣ उभरत ह जसक क ध भ \ ब झ स झ क चक ɇऔर द श ȧ \ ǓȲ ` à Ȣ ह न क न त Ȣतरह खद क \ ǔè क बन ए ह ए ह, ȯ कम ह त è ȡèØ बजट स कभ कभ f à ȧ ȡȲ Ʌभ अटक ज त ɇ@ऐस म ह ल Ʌ Ȫ ȣ ȯ ` ȡ कदम ह जसक ब हतर ȢǓ ȡ ȡ[Û ȡ [ Ǔ è ȡèØ स व ओ ȧ ȣ बदल द ग 1 ȡ ȡȲ Ǔ Ȣ \ è ȡ इस Ĥ ȡ क å ȡ क उनक ɮ ȡ ȡ f गए ȡ ȣǔ ȯ ȧ ǗǓ [करन क f ज यज ठहर त ɇ, ȯ उसक f ȡ[Ü समय द न क र ज ȣȳ ɇ@ǔ ȯ ȧगई ȡ Ǘ ȣह ज न क ब वजद ȡ ȣमन फ वसल न क यह ȡ ȡ è Ǘ ȡ ȣ ȣरहन व ल ह इस è ȡस बचन क f सरक र क ǔþ Ĥȡ^ ȯ ȡ [ (प प प ) म डल क \ è ȡ ɉ क बढ़ व द न पर ȡ करन ȡǑ f जसस Ǔ ȯ ȧल गत स Ǔ Ȣ Ȳè ȡ भ बच Ʌऔर ब क ब \ è ȡ ɉपर लग म भ लग सक

23 National Health Protection Scheme (Hindustan: )

24 Mini Tumour (Hindustan: )

25 Arthritis (Dainik Jagran: )

26 Garmunda Flower (Dainik Jagran: )