Category Archives: Genetic Medicine

By: Editorial | Updated: February 10, 2020 9:10:58 am Global science would also benefit from a mapping project in one of the worlds most diverse gene pools, which would provide data useful for the mapping of the spread and migration of a range of life forms in the Old World, from plants to humans.

The Genome India Project, a collaboration of 20 institutions including the Indian Institute of Science and some IITs, will enable new efficiencies in medicine, agriculture and the life sciences. The first obvious use would be in personalised medicine, anticipating diseases and modulating treatment according to the genome of patients. Several diseases develop through metabolic polymorphisms the interplay of the environment with multiple genes, which differ across populations. For instance, one group may develop cancers and another may not, depending on the genetically-determined pathways by which they metabolise carcinogens. Cardiovascular disease generally leads to heart attacks in South Asians, but to strokes in most parts of Africa. If such propensities to disease can be mapped to variations across genomes, it is believed public health interventions can be targeted better, and diseases anticipated before they develop. Similar benefits would come to agriculture if there is a better understanding of the genetic basis of susceptibility to blights, rusts and pests. It may become possible to deter them genetically, and reduce dependence on chemicals.

Global science would also benefit from a mapping project in one of the worlds most diverse gene pools, which would provide data useful for the mapping of the spread and migration of a range of life forms in the Old World, from plants to humans. Traversing from the worlds tallest mountain range to warm seas through multiple bio-zones demarcated by climate and terrain, India could provide much information on the interplay of species and genetic groups within them. Eventually, a deeper understanding of ecology could emerge from the material thrown up.

However, some caution must be exercised in the field of human genetics, because the life sciences sometimes stray into unscientific terrain and heighten political bias. The mapping of brain regions to mental functions spun off the utterly unscientific and racist field of phrenology. The work on cranial volume measurements of the physician Samuel Morton regarded in America as the father of scientific racism justified slavery before the US Civil War. In India, a nation riven by identity politics and obsessed with the myths of pristine origins and authenticity, scientific work in mapping genetic groups may become grist to the political mill of the unscientific notion of race. Projects in genetics generally extend over long periods of time, which should be used by makers of scientific policy to ensure that the data which emerges is not interpreted for political ends.

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Mapping life - The Indian Express

A scaly animal that is one of Asias most illegally trafficked mammals may have spread the coronavirus to humans, according toa Chinese university.

So far, the coronavirus has infected more than 31,000 people in China, and the death toll has surpassed 630 since the outbreak started in Wuhan in December. Its believed to have been passed to humans at a seafood and wild-animal market.

The coronavirus is believed to have originated in bats and transferred to humans through some other animal. Now researchers at the South China Agricultural University say the pangolin, a mammal illegally trafficked in large numbers for its scales and meat, may be the link.

This latest discovery will be of great significance for the prevention and control of the origin of the new coronavirus, South China Agricultural University said in a statement.

Researchers said they found a 99 percent match between the genome sequences of viruses in pangolins and those in human patients after testing more than 1,000 samples from wild animals, the AFP reported.

But other scientists are questioning the research. Scientists say the suggestion based on a genetic analysis seems plausible, but caution that the researchers work is yet to be published completely.

This is an extremely interesting observation. Although we need to see more details, it does make sense as there are now some other data emerging that pangolins carry viruses that are closely related to 2019-nCoV. Edward Holmes, an evolutionary virologist at the University of Sydney, Australia said in Nature.

Other independent scientists said much more information is needed before a conclusion can be drawn. James Wood, head of the veterinary medicine department at Britain's University of Cambridge, told Reuters the research was far from robust.

"The evidence for the potential involvement of pangolins in the outbreak has not been published, other than by a university press release. This is not scientific evidence," Wood told Reuters.

Pangolins, the worlds only scaly mammal, are protected animals but are illegally trafficked in large numbers,with some species are critically endangered. They are sought after for their meat and scales, which are used in traditional Chinese medicine.

Originally posted here:
Pangolins may have spread the coronavirus to humans - The Hill

07 Feb 2020

ApoE4s rap sheet just grew longer. Not only does ApoEs notorious allele accelerate A and tau pathology, it also drives the toxic aggregation of -synuclein, according to two studies published February 5 in Science Translational Medicine. One was led by Guojun Bu at the Mayo Clinic in Jacksonville, Florida; the other, by David Holtzman at Washington University in St. Louis. Both reported that ApoE4 aggravated -synuclein phosphorylation, worsened motor and memory problems, and ramped up neurodegeneration in different mouse models. Once again, the goody-two-shoes allele, ApoE2, was protective, Holtzman and colleagues reported. People with Lewy body dementia who inherited an ApoE4 allele had more phosphorylated -synuclein and faster cognitive decline than noncarriers.

Patrik Brundin of the Van Andel Research Institute in Grand Rapids, Michigan, said the studies further blur the line between Alzheimers and Lewy body dementias, in terms of both genetic risk and neuropathology. The findings suggest that there might be opportunities to develop [single] therapies that target more than one of these neurodegenerative disorders in the future, he wrote.

Dementia with Lewy bodies (DLB) and Parkinsons disease dementia (PDD) both fall under the umbrella of Lewy body dementias (LBDs), which hit patients with a double whammy of movement problems and cognitive impairment. Lewy bodies chock-full of aggregated -synuclein underlie these disorders, but many people with LBD also have A and tau pathology.

ApoE4, the strongest genetic risk factor for late-onset Alzheimers, also increases the risk for cognitive decline in people with PD, and is a risk factor for DLB as well (Mata et al., 2014;Dec 2015 news; Guerreiro et al., 2018). Studies hinted that in LBDs, ApoE4 works in much the same way as it does in AD, by ramping up A and/or tau pathology (Irwin et al., 2017; Sep 2016 news). However, others have reported that ApoE4 promotes -synuclein pathology independently (Tsuang et al., 2013;Dickson et al., 2018).

To directly assess this, researchers led by Bu used a mouse model of synucleinopathy. First author Na Zhao injected adeno-associated viruses expressing human -synuclein into both lateral ventricles of newborn ApoE-targeted replacement mice. These express human ApoE2, ApoE3, or ApoE4in place of the endogenous mouse gene.

Nine months later, the scientists used two antibodiesone that recognizes pathological conformations of -synuclein in people with LBD, and the other specific for -synuclein phosphorylated at serine-129to measure -synuclein pathology in multiple brain regions. They found roughly double the amount of both pathological conformers and phosphorylated -synuclein in several brain regions of Syn-ApoE4 compared with Syn-ApoE2 or Syn-ApoE3 mice. Immunoreactivity of the two antibodies correlated tightly.

This uptick in -synuclein pathology had consequences. All the Syn mice were unbalanced and uncoordinated compared with controls, but ApoE4 mice fared worst. They also spent more time in an exposed area, suggesting they had lost some of their normal fear and inhibition. While Syn-ApoE2 and Syn-ApoE3 mice readily remembered sounds that signaled an impending foot shock, Syn-ApoE4 mice had trouble on this memory task.

Normal neuron and synaptic protein levels in E2 and E3 mice stood in contrast to 10 percent fewer neurons in ApoE4s and a dip in levels of the postsynaptic protein PSD95. E4 mice had astrogliosis and microglial activation that were absent in Syn mice expressing the other alleles. However, the researchers found no correlation between the burden of pathological conformers of -synuclein in a given mouse and its degree of astrogliosis or microglial activation, suggesting the stepped-up neuroinflammation in ApoE4 mice was unrelated to the increased -synuclein pathology.

A transcriptomic analysis revealed lower expression of genes involved in lipid metabolism and less glycogen synthase activity in ApoE4 mice, as well as suppression of genes needed for synaptic signaling, protein metabolism, and social behavior.

Does ApoE4 influence -synuclein pathology in LBD? To find out, Zhao and colleagues measured pathologic conformations and p-Ser129 -synuclein in postmortem brain samples from 44 people who had had pure LBD with little to no A pathology. Half were ApoE4 carriers. On average, they had more p-Ser129 -synuclein than age-matched noncarriers, but not more of the pathological conformation. The researchers detected no differences in astrocytic or microglial markers between carriers and noncarriers, nor did glial activation markers correlate with the burden of p-Ser129 -synuclein across all participants. Together, these findings suggested that ApoE4 exacerbates -synuclein pathology in people with LBD but does not necessarily stoke neuroinflammation.

Bu said the lack of a direct link between the burden of -synuclein pathology and glial activation was unsurprising. As an intracellular protein, -synuclein is less likely to incite glial cells than extracellular aggregates, such as A.

Revving Up Syn. Postmortem brain samples of LBD patients indicate that ApoE4 carriers (bottom) had more phosphorylated -synuclein than did noncarriers. [Courtesy of Zhao et al., Science Translational Medicine, 2020.]

In the second paper, first author Albert Davis and colleagues used a different mouse. They crossed A53T-Syn transgenic mice with the same ApoE-targeted replacement mice Bu and colleagues used. Compared with the viral approach, the A53T-Syn mice develop more severe disease, becoming paralyzed by 12 months of age. While Bus injected mice had -synuclein pathology in many brain regions, the vast majority of -synuclein inclusions in the A53T-Syn mice developed in the brainstem, with sparse pathology in the neocortex.

Analyzing brainstem lysates from 12-month-old mice, Davis detected the highest levels of insoluble -synuclein, as well as p-Ser129 -synuclein, in ApoE4 mice. ApoE3 and ApoE knockouts had progressively less, and in lysates from ApoE2 mice, insoluble and phosphorylated forms of -synuclein were virtually undetectable. Immunohistochemistry of brainstem sections told a similar story, with ApoE2 mice having no detectable phosphorylated -synuclein, while ApoE4 had the most. Interestingly, p-Ser129 -synuclein only appeared in mice with end-stage paralysis, which afflicted many ApoE4 and ApoE knockout mice by 12 months of age. ApoE2 mice did not develop severe paralysis until much later, around 18 months, suggesting that the allele staved off both -synuclein pathology and neurodegeneration.

The scientists also compared transcriptomes. Both the amount of -synuclein pathology and end-stage paralysis tracked with higher expression of proinflammatory genes, but not with ApoE genotype alone. This suggested that neuroinflammation arose in response to -synuclein pathology and neurodegeneration, as opposed to being caused by ApoE4. Davis also picked up modules of myelination and anti-apoptotic genesthese were more highly expressed in ApoE2 mice.

Compared with Bus study, Davis found stronger ties between the burden of -synuclein pathology and neuroinflammation. The reason for this discrepancy is unclear, but both researchers believe it could come down to differences between mouse models. Because the A53T-Syn mice express much higher levels of -synuclein than the virally infected model, the former could evoke a more pro-inflammatory component, Bu suggested.

ApoE Impacts Syn. Brainstem sections reveal the most p-Ser129 -synuclein pathology (red) and astrogliosis (green) in ApoE4 mice; ApoE2 mice had neither. [Courtesy of Davis et al., Science Translational Medicine, 2020.]

Davis next investigated the relationship between ApoE genotype and cognition in several cohorts of PD patients. Among 251 people with PD in the Parkinsons Progression Markers Initiative, the researchers found faster decline on the Montreal Cognitive Assessment in the ApoE4 carriers. While people with abnormal CSF A42 or p-tau also declined faster on this screen, ApoE4 correlated independently. In two other PD cohorts, the researchers found ApoE4 carriers declined more sharply on the mini-mental state examination.

While the two papers came to slightly different conclusions in some respects, their main conclusion was the same, Bu said: ApoE4 can drive -synuclein pathology in the complete absence of amyloid.

Exactly how ApoE does that remains unclear. ApoE is an extracellular protein, whereas the vast majority of -synuclein resides inside, attached to synaptic vesicles. Still, small pools of -synuclein have been detected outside of cells and, when aggregated, it can spread between neurons via a templated misfolding mechanism, at least in mice. It is possible the two lipophilic proteins meet up in this extracellular milieu, Bu said. In support of this, Davis also reported that preformed fibrils of -synuclein injected into the mouse striatum spread more readily into neighboring substantia nigra when the animals expressed ApoE4.

Thomas Montine of Stanford University favors the idea that ApoE isoforms sway -synuclein aggregation indirectly, via their role as immune modulators. He noted that, in general, ApoE4 promotes pro-inflammatory responses, while ApoE2 does the opposite.

If ApoE4 drives -synuclein aggregation, then why is it a risk factor for LBD, but not PD? Davis said the answer could come down to where in the brain ApoE4 influences -synuclein aggregation. Perhaps the allele is most impactful in cortical and limbic regions involved in cognition, he speculated. These regions are more affected by -synuclein pathology in LBD than in PD, in which -synuclein aggregates primarily pop up in the midbrain. Davis plans to use mouse models with more widespread -synuclein aggregation to investigate this. Montine concurs that neuropathological studies suggest that ApoE4 strongly affects -synuclein aggregation in cortical and limbic regions (Dickson et al., 2018). Another possibility is that ApoE4 promotes the propagation of -synuclein pathology from the midbrain into these areas, Davis said.

Despite myriad unknowns, the new findings cast ApoE as a potential therapeutic target not only in AD, but also in LBD, Bu and Davis agreed. Montine noted that the protective effect of ApoE2 reported in Daviss study is important, especially in light of recent reports that the allele strongly protects against AD (Feb 2020 news). A therapy that mimics the behavior of ApoE2 could benefit patients with LBD and AD, he said.Jessica Shugart

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Toxic -Synuclein: Egged on by ApoE4, Thwarted by ApoE2? - Alzforum

Before 2011, if you had chest pain and went to what was then Great Plains Regional Medical Center, theyd run non-invasive tests, like an echocardiogram.

If you showed signs of a heart attack, youd probably be given a medication that dissolves blood clots and then flown to a larger hospital. That medication, called a thrombolytic, can restore blood flow to the heart in most people. But time is muscle, and if flow isnt completely restored, there can still be muscle loss.

Maybe you wouldnt even go to Great Plains for medical help, as was noted in a Sept. 1987 Telegraph article: Although the hospital has equipment and qualified doctors to provide heart tests, heart patients often leave North Platte.

There are a fair number who leave town because we dont have a cardiologist, (hospital president Cindy) Bradley said.

The hospital had a cardiac rehabilitation lab for people after they have a heart attack, but little to do to prevent or treat one.

In a county with one of the highest death rates due to cardiovascular disease in the state, the hospitals board decided in 2004 that something needed to be done to establish cardiovascular care in Lincoln County.

It began with a diagnostic catheterization lab: A place where tests can be done to determine if intervention is needed.

Patients who didnt have an active heart attack would be given a general cardiology work-up, which generally included an electrocardiogram measuring the electrical activity of the heartbeat and maybe a diagnostic catheterization passing a thin, flexible tube through the vessels in the heart to see how well the organ is functioning. Patients with a heart attack would be transferred to another hospital with treatment options.

Ivan Mitchell

As you can see, we had a lot of good diagnostic tools, but no intervention tools, said Ivan Mitchell, chief operating officer of Great Plains Health. With time being muscle for your heart, it took a lot longer to do treatment.

Cardiologys roots run deep

Humans have realized the importance of the pulse and the heart since ancient times: An unknown Egyptian physician describes the heart as the center of a system of vessels and seems to identify arterial fibrillation, a condition where the heart fails to beat with enough force to pump blood and that can cause cardiac arrest, according to a 1995 paper by Dr. James Willerson and Rebecca Teaff.

In the fourth century B.C., the philosopher Aristotle thought that the heart was the seat of intelligence, whereas the brain merely existed to cool blood.

In the second century A.D., the prominent physician Galen cited the liver as the source of veins, and said the heart was simply an organ blood passed through.

It wasnt until 1628 that the heart came back into the spotlight as the organ responsible for circulation. At that time, English physician William Harvey published his key work, in which he proposed that the heart pumps blood around the body with a single system of arteries and veins. The book included experiments and evidence backing that up, though others in the field were slow to accept his idea.

It took until the 20th century for physicians to link chest pain and hardening of the arteries with heart attacks, according to Dr. Rachael Hajar in her 2017 article on the history of coronary artery disease.

Getting blood pumping in the Great Plains

In 2011, the GPH board decided to move toward an interventional program they wanted to treat people right then and there if they came into the hospital with a heart attack.

They hired on a doctor, and added an interventional cath lab and clinic space. They added another doctor.

And then something happened.

What was really interesting was that we started to see the mortality rate decrease when that happened, Mitchell said, because if someone has an active heart attack, (the cardiology team) could do an intervention essentially right away.

The program couldnt seem to stop growing a second cath lab had to be added in 2018, and more doctors were hired.

Since 2016, weve had about 300% growth, Mitchell said. Weve really become a regional presence and referral center for our cardiology program.

The lab is a really, extremely busy cath lab, with 11 procedures alone taking place on the day Mitchell was interviewed.

The interventions include implantable medical devices, like the implantable cardiovascular defibrillator a battery-powered device that keeps track of heart rate and pacemakers, which help the heart beat in a regular rhythm. Even after the patient leaves the hospital with an implantable device, theyll still receive support from what Mitchell calls the Device Clinic.

If you have a pacemaker in and your heart throws a rhythm thats concerning, it will actually alert our Device Clinic, which will then alert the physicians, he said. Having that (clinic) here has been a great thing.

With all of the procedures available at GPH, some may be surprised to learn that the hospital doesnt have a cardiothoracic surgeon on site.

The data out there suggest that the programs without cardiothoracic surgery in hospitals have just as good of outcomes as programs that do have cardiothoracic surgery, Mitchell said. So what weve done is if someone comes in and their blockage is so severe that they need open heart surgery, we actually have a couple of tools that are used (until they can be transferred).

One of those options is a balloon pump, which is a balloon attached to a catheter. The doctor inserts it into the artery inside your upper leg and guides it to the aorta, or main artery, where the balloon inflates when the heart relaxes and deflates when it contracts. This allows the heart to pump more blood to the body using less energy, according to Johns Hopkins Medicine.

The other option is a device called an Impella, a mini heart pump that goes in like the balloon pump and works by drawing blood out of the heart and pumping it into the aorta, according to the Federal Drug Administrations page on recently approved medical devices.

(Acute interventions) really save lives, without any question, said Dr. Azariah Kirubakaran, an interventional cardiologist at GPH.

Until 1961, heart attack patients who made it to a hospital were simply placed in beds located throughout the hospital, far away from nurses stations, often with lethal results the risk of dying in a hospital from myocardial infarction was around 30%, according to Nabel and Braunwald.

Following that, cardiac care units where heart attack patients were closely monitored were implemented in general hospitals.

Balloon angioplasty and insertion of bare-metal stents were implemented soon after.

The first artery-to-artery anastomosis, known today as a cardiac bypass graft surgery, was performed in 1968 by Dr. George Green of Saint Lukes Hospital in New York. This surgery has become the absolute gold standard for bypasses, said Ludovic Melly and Gianluca Torregrossa in a 2018 article on the history of artery bypass grafting.

Cardiologists began to open blocked coronary arteries using streptokinase, a thrombolytic, in 1976.

In 1988, it was found that aspirin further reduced deaths in patients who had suffered heart attacks when used in conjunction with a thrombolytic.

These leaps and bounds in treatment are so recent that Kirubakaran can recall what he calls the dark ages during the early days of his own career.

I have personally seen people just die like flies, basically, back in the 80s, when they had heart attacks, Kirubakaran said. Compared to that, its a night and day difference. Even though I cant say that nobody dies of a heart attack thats not true the risk has been tremendously reduced with all the technologies we have, and its getting better every year.

For as many patients who have sought treatment, GPH is also trying to make sure some patients dont get to that point.

Dr. Azariah Kirabakaran

(Prevention) is a lot more attractive than trying to fix something once its happened for a variety of reasons: One, it doesnt put patients at risk at the time of the expression of the disease, Kirubakaran said. Secondly, its a lot less expensive to do so. And now there are ways of prevention that can be applied to large populations and it can be helpful to do so.

The Heart Institute at GPH has started offering a discounted cardiac screening to help patients determine their risks.

There are a lot of people who theyve caught those heart issues early on because of (the screenings), Mitchell said.

One of the components of that screening is calcium scoring, which measures the build-up of calcium in arteries. The greater the amount of calcified plaque, the higher the risk of heart disease.

But one of the most mundane things is also one of the best ways to catch heart problems early.

The most basic thing is to get your physical: Check your bloodwork, check your blood pressure, all that good stuff, Mitchell said. Ensuring that youre established with your primary care provider is also important because they can track your health over time and identify any worrying trends.

In spite of all of the treatment, diagnostic and preventative measures, Kirubakaran and Mitchell still feel that the program has more room to grow.

Kirubakaran hopes the program will be able to move toward doing more than just treating blockages with catheters.

We can replace some other valves at least with catheter-based techniques, which are a lot less invasive. It can be tolerated even by people who are very, very frail. Even seven or eight years ago, that was something unimaginable, but now its almost routine, Kirubakaran said.

Another thing that Kirubakaran hopes to see is cardiac MRI, which would allow them to see the heart in greater detail.

Studies show that the MRI is probably a lot more acurate of a stress test than any other test we can run. he said.

Mitchell also spoke on the possibility of eventually bringing an electrophysiologist to GPH, someone who would deal with electrical impulses in the heart and would be able to burn or scar heart tissue causing irregular heartbeats, a procedure known as an ablation. Much like in a house, one person cant necessarily fix everything.

Your interventional cardiologist is like a plumber theyre making sure the pipes are working and that the blood is pumping through your system, Mitchell said. An electrophysiologist is considered the electrician, and theyre making sure the rhythm is proper.

Technological advances are changing the ways cardiovascular disease is approached.

Kirubakaran described a medication being developed that would lower bad cholesterol by 40% to 45% with a single shot once a year.

A lot of people are already looking at it in terms of preventing large populations of people (from further developing heart disease), Kirubakaran said. It turns out that the longer your blood vessels are exposed to bad cholesterol, the higher the liklihood of developing a blockage. Being able to reduce the amount of bad cholesterol would therefore reduce the risk.

The Human Genome Project, where researchers sequenced and mapped all of the genes in Homo sapiens, was completed in 2003 and gave more insight into genetic components of diseases. Kirubakaran discussed the implications this research has in treatment of cardiovascular disorders.

Now there are a lot of things we know about atrial fibrillation, congestive heart failure, coronary artery disease, cardiomyopathy these all have some genetic background to them. How much genetics has a role to play and how much environment has a role to play, those are variable depending on an individual patient, Kirubakaran said. But now we are having more and more success figuring out how much genetics is playing a role, which can lead to better therapies that target the genes causing the diseases.

Kirubakaran is looking to a future without heart attacks.

Once theres a heart attack, its a messy thing. Theres no easy, clear-cut solution, Kirubakaran said. So if my patients never get to that point, Ill be really happy.

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At the heart of our own history: Cardiology sees changes in North Platte and beyond - North Platte Telegraph

Express News Service

There is so much we can do beyond medicine for our health and well-being. Let medicines do their work but, there are plenty of other tools that can improve our quality of life. One such tool is prayer, provided it is done the right way. Neither do you have to be a religious person nor do you need to visit a religious place to do a prayer. This is about honest spirituality and true prayer is free from all of this.

How do prayers work: Everything is energy. The food you eat, the water you drink, the air you breathe. We ourselves are a bundle of energy. We can create bad or good energy. Prayer done with a clean heart and intentions helps generate good energy or change the bad energy into good energy. So, imagine the amount of good energy you can create by praying and how that can be channelised for healing.

Prayers can affect us at a genetic level: They have the ability to awaken certain emotions in our system that has the ability to turn on and turn off certain genes. Our lifestyles have a huge role to play here. While clean lifestyle habits can turn on genes that have the ability to repair and heal you, unhealthy lifestyle habits can turn on genes that can bring about sickness and diseases. This is called epigenetics, where epi stands for the environment and how it can control the functionality of a certain gene. For example: watching a clip of a funny video, movie or a good laugh with friends can turn on over 700 genes that are related to our immune system. But a drag, anxious and angry lifestyle can also turn off those same 700 genes thereby dampening your immunity. Prayers work in a similar way, by evoking positive emotions in us that has the capacity to activate the good genes.

Why do most patients who have gone through their journey of cancer turn to spirituality? There are some who never ever prayed in their life but have now come down to praying heavily. What changes? Well, as the mysteries of life unfold and the journey gets challenging, most individuals tend to go through intense emotions of love, lost love, relationship issues, unforgiveness, anger and shifting their focus towards spirituality and prayer asking for safety and recovery. And it doesnt take a disease to lead to this. As kids and teens, visiting holy places disinterest us, then as we grow older, we gradually move to read holy books and spend time chanting. Some people experience this transition early in life and some later.

We go wrong when spirituality is practiced as a fad and we add more complexity to it. Prayers are not any other to-do list activity in your day. If you pray, let those prayers and their teachings slip into your daily life. The three most essentials when it comes to prayers is Faith, Belief, and Surrendering. So many of us pray fervently almost daily, visit different religious places, but are still anxious and worried about the very problems they prayed for. Instead, pray with utmost faith and belief and just surrender the outcome. Above all, keep practicing your prayers till you build so much faith that there is no room for fear.

The simplest prayer: The simplest one could be to offer gratitude and count your blessings. It doesnt have to be a prayer for God. Prayer in any form, if done with faith and belief, counts. For example: Thank you for blessing the air that we breathe, the food that we eat and the water that we drink. Just because the results of prayers arent immediate doesnt mean its not powerful. The power of this simple act is immense, free and we mustnt take for granted what is free. Sometimes when life hits us through any challenge, financial, emotional, physicalall we need to do is step back, pray and ask for help. Teach this to your kids too.

The author is a Mumbai-based holistic lifestyle coach

Luke Coutinho

See the rest here:
The power of prayers - The New Indian Express

If you are looking to grow your skills or wondering what to study, you may want to focus on subjects that could help you land jobs that are likely to grow quickly in the next few years.

Every two years, the US Bureau of Labor Statistics releases employment projections, estimating how employment in various occupations is likely to grow over the next decade. The most recent projections include a list of the fastest-growing occupations based on the estimated employment change between 2018 and 2028. To determine what changes in occupational employment may look like over 10 years, the BLS used various resources like historical data and scholarly papers.

According to the BLS, two of the broad occupational groups that will be quickly growing are healthcare support, with an expected increase in employment of 18.2%, followed by personal care and services, where employment is projected to grow by 17.4%. Jobs that are predicted to grow within these occupation categories include various kinds of healthcare aides, physician assistants, and nurse practitioners.

To get a sense of what skills are most important to the fastest-growing jobs, we used the Labor Department's Occupational Information Network (O*NET) importance scales regarding skills and knowledge. Based on surveys of employers and workers, these scores range from 0 to 100, where a higher score indicates a more important skill or knowledge area for a particular job.

We looked at the top three skills and knowledge areas for each of the 15 jobs with the highest projected employment growth between 2018 and 2028. Occasionally, there were ties among the top three most important skills and knowledge areas.

For the fastest-growing occupations, there was some overlap in the kinds of skills and knowledge areas that are important to fulfilling job responsibilities. Active listening was the most frequently listed skill among the top three in the 15 fastest-growing jobs, while understanding English and psychology were the top knowledge fields.

It's worth notingthat these skills are non-technological ones O*NET has a separate technology skills section. Although it may be important to have a background in various technology applications, it is interesting to see which social or conceptual skills employees and workers find important in order to succeed in their jobs.

Read on to find out the 15 projected fast-growing jobs between 2018 and 2028, along with their growth rate, average salary in 2018, top skills and knowledge areas, and job description according to O*NET.

Original post:
The skills and knowledge you need to succeed in the fastest-growing jobs in America - Business Insider - Business Insider