Scratching the surface of how your brain senses an itch

Light touch plays a critical role in everyday tasks, such as picking up a glass or playing a musical instrument. The sensation is also an essential part of the body’s protective defense system, alerting us to objects in our environment that could cause us to fall or injure ourselves. In addition, it is part of the detection system that has evolved to protect us from biting insects, such as those that cause malaria and Lyme disease, by eliciting a feeling of an itch when an insect lands on your skin.

Salk researchers have discovered how neurons in the spinal cord help transmit such itch signals to the brain. Published in the journal Cell Reports on July 16, 2019, their findings help contribute to a better understanding of itch and could lead to new drugs to treat chronic itch, which occurs in such conditions as eczema, diabetes and even some cancers.

“The takeaway is that this mechanical itch sensation is distinct from other forms of touch and it has this specialized pathway within the spinal cord,” says Salk Professor Martyn Goulding, holder of the Frederick W. and Joanna J. Mitchell Chair and a senior author of the new work.

Goulding and his colleagues had previously discovered a set of inhibitory neurons in the spinal cord that act like cellular brakes, keeping the mechanical itch pathway in the spinal cord turned off most of the time. Without these neurons, which produce the neurotransmitter neuropeptide Y (NPY), the mechanical itch pathway is constantly on, causing chronic itch. What the researchers didn’t know was how the itch signal, which under normal circumstances is suppressed by the NPY neurons, is transmitted to the brain to register the itch sensation.

David Acton, a postdoctoral fellow in the Goulding lab, hypothesized that when the NPY inhibitory neurons are missing, neurons in the spinal cord that normally transmit light touch begin to act like an accelerator stuck in the “on” position. Acton then identified a candidate for these “light touch neurons,” a population of excitatory neurons in the spinal cord that express the receptor for NPY, the so-called Y1 spinal neurons.

To test whether these neurons were indeed acting like an accelerator, Acton undertook an experiment that involved selectively getting rid of both the NPY “brake” and Y1 “accelerator” neurons. Without Y1 neurons, mice didn’t scratch, even in response to light-touch stimuli that normally make them scratch. Moreover, when Acton gave the animals drugs that activated the Y1 neurons, the mice scratched spontaneously even in the absence of any touch stimuli. The Goulding team was then able to show that the NPY neurotransmitter controls the level of Y1 neuron excitability; in other words, NPY signaling acts as a kind of thermostat to control our sensitivity to light touch. Data from other labs has found that some people with psoriasis have lower than average levels of NPY. This may mean their brakes on mechanical itching are less effective than other people’s, a potential cause of their itching.

While Y1 neurons transmit the itch signal in the spinal cord, other neurons are thought to be responsible for mediating the final response in the brain but more research is needed to continue mapping out the full pathway, according to the researchers. Understanding this will help suggest targets for drugs to turn down the sensation of itch in people who are overly responsive and could lead to ways to address chronic itch.

“By working out mechanisms by which mechanical itch is signaled under normal circumstances, we might then be able to address what happens in chronic itch,” says Acton.

Other researchers on the study were Xiangyu Ren, Stefania Di Costanzo, Antoine Dalet and Steeve Bourane of the Salk Institute; and Ilaria Bertocchi and Carola Eva of the University of Torino.

The study was supported by the National Institutes of Health and the Caterina Foundation.

Story Source:

Materials provided by Salk InstituteNote: Content may be edited for style and length.


Journal Reference:

  1. David Acton, Xiangyu Ren, Stefania Di Costanzo, Antoine Dalet, Steeve Bourane, Ilaria Bertocchi, Carola Eva, Martyn Goulding. Spinal Neuropeptide Y1 Receptor-Expressing Neurons Form an Essential Excitatory Pathway for Mechanical Itch

Scorpion toxin that targets ‘wasabi receptor’ may help solve mystery of chronic pain

 

 

Researchers at UC San Francisco and the University of Queensland have discovered a scorpion toxin that targets the “wasabi receptor,” a chemical-sensing protein found in nerve cells that’s responsible for the sinus-jolting sting of wasabi and the flood of tears associated with chopping onions. Because the toxin triggers a pain response through a previously unknown mechanism, scientists think it can be used as a tool for studying chronic pain and inflammation, and may eventually lead to the development of new kinds of non-opioid pain relievers.

The scientists isolated the toxin, a short protein (or peptide) that they dubbed the “wasabi receptor toxin” (WaTx), from the venom of the Australian Black Rock scorpion. The discovery came as the researchers were conducting a systematic search for compounds in animal venom that could activate, and therefore be used to probe and study, the wasabi receptor — a sensory protein officially named TRPA1 (pronounced “trip A1”) that’s embedded in sensory nerve endings throughout the body. When activated, TRPA1 opens to reveal a channel that allows sodium and calcium ions to flow into the cell, which can induce pain and inflammation.

“Think of TRPA1 as the body’s ‘fire alarm’ for chemical irritants in the environment,” said John Lin King, a doctoral student in UCSF’s Neuroscience Graduate Program and lead author of a study published August 22, 2019 in Cell, which describes the toxin and its surprising mode of action. “When this receptor encounters a potentially harmful compound — specifically, a class of chemicals known as ‘reactive electrophiles,’ which can cause significant damage to cells — it is activated to let you know you’re being exposed to something dangerous that you need to remove yourself from.”

Cigarette smoke and environmental pollutants, for example, are rich in reactive electrophiles which can trigger TRPA1 in the cells that line the surface of the body’s airway, which can induce coughing fits and sustained airway inflammation. The receptor can also be activated by chemicals in pungent foods like wasabi, onions, mustard, ginger and garlic — compounds that, according to Lin King, may have evolved to discourage animals from eating these plants. WaTx appears to have evolved for the same reason.

Though many animals use venom to paralyze or kill their prey, WaTx seems to serve a purely defensive purpose. Virtually all animals, from worms to humans, have some form of TRPA1. But the researchers found that WaTx can only activate the version found in mammals, which aren’t on the menu for Black Rock scorpions, suggesting that the toxin is mainly used to ward off mammalian predators.

“Our results provide a beautiful and striking example of convergent evolution, whereby distantly related life forms — plants and animals — have developed defensive strategies that target the same mammalian receptor through completely distinct strategies,” said David Julius, PhD, professor and chair of UCSF’s Department of Physiology, and senior author of the new study.

But what the researchers found most interesting about WaTx was its mode of action. Though it triggers TRPA1, just as the compounds found in pungent plants do — and even targets the very same site on that receptor — the way it activates the receptor was novel and unexpected.

First, WaTx forces its way into the cell, circumventing the standard routes that place strict limits on what’s allowed in and out. Most compounds, from tiny ions to large molecules, are either ingested by the cell through a complex process known as “endocytosis,” or they gain entry by passing through one of the many protein channels that stud the cell’s surface and act as gatekeepers.

But WaTx contains an unusual sequence of amino acids that allows it to simply penetrate the cell’s membrane and pass right through to the cell’s interior. Few other proteins are capable of the same feat. The most famous example is an HIV protein called Tat, but surprisingly, WaTx contains no sequences similar to those found in Tat or in any other protein that can pass through the cell’s membrane.

“It was surprising to find a toxin that can pass directly through membranes. This is unusual for peptide toxins,” Lin King said. “But it’s also exciting because if you understand how these peptides get across the membrane, you might be able to use them to carry things — drugs, for example — into the cell that can’t normally get across membranes.”

Once inside the cell, WaTx attaches itself to a site on TRPA1 known as the “allosteric nexus,” the very same site targeted by pungent plant compounds and environmental irritants like smoke. But that’s where the similarities end.

Plant and environmental irritants alter the chemistry of the allosteric nexus, which causes the TRPA1 channel to rapidly flutter open and closed. This allows positively charged sodium and calcium ions to flow into the cell, triggering pain. Though both ions are able to enter when TRPA1 is activated by these irritants, the channel exhibits a strong preference for calcium and lets much more of it into the cell, which leads to inflammation. By contrast, WaTx wedges itself into the allosteric nexus and props the channel open. This abolishes its preference for calcium. As a result, overall ion levels are high enough to trigger a pain response, but calcium levels remain too low to initiate inflammation.

To demonstrate this, the researchers injected either mustard oil, a plant irritant known to activate the wasabi receptor, or WaTx into the paws of mice. With mustard oil, they observed acute pain, hypersensitivity to temperature and touch — key hallmarks of chronic pain — and inflammation, as evidenced by significant swelling. But with WaTx, they observed acute pain and pain hypersensitivities, but no swelling.

“When triggered by calcium, nerve cells can release pro-inflammatory signals that tell the immune system that something’s wrong and needs to be repaired,” Lin King said. “This ‘neurogenic inflammation’ is one of the key processes that becomes dysregulated in chronic pain. Our results suggest that you can decouple the protective acute pain response from the inflammation that establishes chronic pain. Achieving this goal, if only in principle, has been a longstanding aim in the field.”

The researchers believe their findings will lead to a better understanding of acute pain, as well as the link between chronic pain and inflammation, which were previously thought to be experimentally indistinguishable. The findings may even lay the groundwork for the development of new pain drugs.

“The discovery of this toxin provides scientists with a new tool that can be used to probe the molecular mechanisms of pain, in particular, to selectively probe the processes that lead to pain hypersensitivity,” Lin King said. “And for those interested in drug discovery, our findings underscore the promise of TRPA1 as a target for new classes of non-opioid analgesics to treat chronic pain.”

Additional authors include Joshua J. Emrick, Mark J.S. Kelly and Katalin F. Medzihradszky of UCSF; Volker Herzig and Glenn F. King of the Institute for Molecular Bioscience at the University of Queensland.

This study was supported by an NSF Graduate Research Fellowship (No. 1650113), a UCSF Chuan-Lyu Discovery Fellowship, and grants from the National Institutes of Health (R37 NS065071, R35 NS105038 and T32 GM007449).

Story Source:

Materials provided by University of California – San Francisco. Original written by Jason Alvarez. Note: Content may be edited for style and length.


Journal Reference:

  1. John V. Lin King, Joshua J. Emrick, Mark J.S. Kelly, Volker Herzig, Glenn F. King, Katalin F. Medzihradszky, David Julius. A Cell-Penetrating Scorpion Toxin Enables Mode-Specific Modulation of TRPA1 and Pain

What is a normal blood pressure ? And How Messure it Manual ?

What is a normal blood pressure ?

Normal blood pressure is vital to life. Without the pressure that forces our blood to flow around the circulatory system, no oxygen or nutrients would be delivered through our arteries to the tissues and organs.

However, blood pressure can become dangerously high, and it can also get too low.

In this article, we will discuss what blood pressure is, how it is measured, and what the measurements mean for our health.

 

What is blood pressure?

A garden hose

Without a pump or water tank, no water will flow. Hose pipe properties also affect water pressure. Similar principles apply for blood flow.

Blood pressure is the force that moves blood through our circulatory system.

It is an important force because oxygen and nutrients would not be pushed around our circulatory system to nourish tissues and organs without blood pressure.

Blood pressure is also vital because it delivers white blood cells and antibodies for immunity, and hormones such as insulin.

Just as important as providing oxygen and nutrients, the fresh blood that gets delivered is able to pick up the toxic waste products of metabolism, including the carbon dioxide we exhale with every breath, and the toxins we clear through our liver and kidneys.

Blood itself carries a number of other properties, including its temperature. It also carries one of our defenses against tissue damage, the clotting platelets that prevent blood loss following injury.

But what exactly is it that causes blood to exert a pressure in our arteries? Part of the answer is simple – the heart creates blood pressure by forcing out blood when it contracts with every heartbeat. Blood pressure, however, cannot be created solely by the pumping heart.

 

Function

Our circulation is similar to a highly sophisticated form of plumbing – blood has ‘flow’ and arteries are ‘pipes.’ A basic law of physics gives rise to our blood flow, and this law also applies in a garden hose pipe.

Blood flows through our body because of a difference in pressure.

Our blood pressure is highest at the start of its journey from our heart – when it enters the aorta – and it is lowest at the end of its journey along progressively smaller branches of arteries. That pressure difference is what causes blood to flow around our bodies.

Arteries affect blood pressure in a similar way to the physical properties of a garden hose pipe affecting water pressure. Constricting the pipe increases pressure at the point of constriction.

Without the elastic nature of the artery walls, for example, the pressure of the blood would fall away more quickly as it is pumped from the heart.

While the heart creates the maximum pressure, the properties of the arteries are just as important to maintaining it and allowing blood to flow throughout the body.

The condition of the arteries affects blood pressure and flow, and narrowing of the arteries can eventually block the supply altogether, leading to dangerous conditions including stroke and heart attack.

 

Measurement

Lady having her blood pressure checked by a doctor

When the pressure from the arm cuff stops the pulse briefly, it gives the top figure of arterial blood pressure that we are familiar with from medical dramas – for example, “140 over 90”

The device used to measure blood pressure is a sphygmomanometer, it consists of a rubber armband – the cuff that is inflated by hand or machine pump.

Once the cuff is inflated enough to stop the pulsea reading is taken, either electronically or on an analogue dial.

The reading is expressed in terms of the pressure it takes to move mercury round a tube against gravity. This is the reason for pressure being measured using the unit millimeters of mercury, abbreviated to mm Hg.

 

Readings

A stethoscope identifies the precise point when the pulse sound returns and the pressure of the cuff is slowly released. Using the stethoscope enables the person measuring the blood pressure to listen out for two specific points.

Blood pressure readings consist of two figures – the systolic pressure first and the diastolic pressure second. The reading is given as, for example, 140 over 90 mm Hg.

The systolic pressure is the higher figure caused by the heart’s contraction, while the diastolic number is the lower pressure in the arteries, during the brief ‘resting’ period between heartbeats.

 

Ranges

The National Institutes of Health cite normal blood pressure to be below 120 mm Hg systolic and 80 mm Hg diastolic.

However, blood pressure changes naturally, a fact that cardiologists explored while writing about blood-pressure variability in Nature in March 2013:

Blood pressure is characterized by marked short-term fluctuations occurring within a 24-hour period (beat-to-beat, minute-to-minute, hour-to-hour, and day-to-night changes) and also by long-term fluctuations occurring over more prolonged periods of time (days, weeks, months, seasons, and even years).”

The guidelines state that for blood pressures above a figure of 115/75 mm Hg, every rise of 20/10 mm Hg doubles the risk of cardiovascular disease.

The overall guidelines for high blood pressure received an update in November 2017. They allow for earlier intervention.

Since 2017, the American Heart Association (AHA) has advised that people with high blood pressure should receive treatment at 130/80 mm Hg rather than 140/90 mm Hg.

They also removed the “prehypertension” category between 120-139/80-89 mm Hg. A blood pressure reading of 140/90 mm Hg now qualifies as stage II hypertension and not stage I, as it used to be.

This category now forms two separate ranges:

  • elevated blood pressure, from 120-129/less than 80 mm Hg
  • stage I hypertension, from 130-139/80-89 mm Hg

In these new guidelines, the AHA also advises that doctors should only prescribe medication in cases of a previous heart attack or stroke, or in the presence of risk factors for these conditions, such as age, a diabetes mellitus diagnosis, or chronic kidney disease.

Treatment at the earlier stages should instead come mainly through lifestyle changes.

What chronic illnesses are people with HIV more likely to experience?

New research looks into the chronic illnesses that people living with HIV are at most risk of developing.

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New research examines what other illnesses HIV may lead to.

In the United States, over 1 million people are currently living with an HIV infection. Worldwide, 1.8 million people have HIV.

Overall, the incidence of HIV infections has declined over the past few decades. The mortality rate from an acquired immunodeficiency syndrome (AIDS)-related illness fell by nearly 80% since the year 2002, according to some estimates.

Despite these trends, HIV remains a global health priority. Worldwide, the leading cause of death among people with HIV is tuberculosis.

However, in countries such as the U.S. where tuberculosis is uncommon, people with HIV die from other conditions that are not related to the immunodeficiency virus. Conditions include diabetes, kidney disease, liver disease, and cardiovascular conditions.

New research set out to examine more closely the specific conditions that people with HIV are at risk of developing.

Lee Smith, a reader in Physical Activity and Public Health at Anglia Ruskin University in London, United Kingdom, is the senior author of the new review.

The findings appear in the journal Clinical Infectious Diseases.

HIV raises risk of COPD, heart disease

Smith and colleagues carried out a so-called umbrella review “of meta-analyses of observational studies.”

The authors looked at 3,413 studies and included 20 in their assessment.

Smith and team rated the evidence available as “convincing, highly suggestive, suggestive, weak, or nonsignificant.” The 20 studies they assessed included 55 health conditions that people with HIV are living with.

The research found that people with HIV are at significant risk of coughing and breathlessness, chronic obstructive pulmonary disease (COPD), as well as “ischemic heart disease, pregnancy-related mortality, maternal sepsis, and bone fractures.”

The authors write: “These results indicate that even with the high availability of [antiretroviral therapy], [people living with HIV] experience disproportionately more chronic respiratory illness in comparison to seronegative populations.”

Furthermore, the risk of ischemic heart disease among people living with HIV, write the authors, might be due to the higher prevalence of smoking and drug use within this population.

However, they add that this “may also be related to underlying, chronic inflammation and immune activation, combined with coagulation abnormalities and atherosclerosis.”

The study’s senior author comments on the findings, saying, “There has been a major shift in how we view HIV. It is no longer a death sentence but rather a manageable chronic illness.”

“By pooling data from different studies,” Smith continues, “we’ve been able to show for the first time that even with the rise in life expectancy among people living with HIV, this population now seems to be disproportionately affected by chronic illnesses often attributable to lifestyle issues, such as smoking, drug, and alcohol use, or more commonly associated with an older population.”

However, the authors emphasize that they cannot be sure that lifestyle factors cause these conditions.

We’re unable to say for certain which are caused or exacerbated by HIV and its treatment, and which are related to lifestyle.”

Lee Smith

“However, the elevated risk levels highlighted in our study should hopefully lead to further research to improve both the prevention and early detection of these comorbidities in people living with HIV. Public health bodies worldwide should reflect on the

Alcohol may be less harmful for people over 50

A recent study examines the health impact of consuming alcohol at different ages. The authors conclude that, for people over the age of 50, the health risks may be less severe.

Older adult wine

If alcohol does have protective effects, they are not distributed evenly across all ages.

Heavy drinking is linked to a range of serious health consequences.

These include certain cancers, liver and heart disease, and damage to the nervous system, including the brain.

However, as has been exhaustively covered in the popular press, drinking in moderation might have certain health benefits.

A number of studies have concluded that drinking alcohol at a low level could have a protective effect.

One study, for instance, found that light and moderate drinking protected against all-cause mortality, as well as mortality related to cardiovascular disease.

It is no surprise that these stories have been well-received and widely read, but not all researchersagree, and the debate is ongoing. 

A recent study led by Dr. Timothy Naimi, of the Boston Medical Center in Massachusetts, adds further fuel to an already rampant blaze.

The authors take aim at the methodology used in earlier studies, and they published their findings in the Journal of Studies on Alcohol and Drugs earlier this week.

A fresh approach

The researchers argue that the way that earlier studies measured alcohol’s impact on health might be flawed. Specifically, they note that the studies are generally observational and usually recruit participants over the age of 50.

The authors argue that this is problematic because it excludes anyone who might have died due to alcohol before the age of 50. As they dryly point out, “Deceased persons cannot be enrolled in cohort studies.”

Dr. Naimi first outlined his concerns about this inherent selection bias in a paper published in the journal Addiction in 2017.

Those who are established drinkers at age 50 are ‘survivors’ of their alcohol consumption who [initially] might have been healthier or have had safer drinking patterns.”

Dr. Timothy Naimi

According to the authors, almost 40 percent of deaths due to alcohol consumption occur before the age of 50.

This means that the vast majority of research into the potential risks of alcohol do not take these deaths into account and could underestimate the real dangers.

To reinvestigate, the authors dipped into data from the Alcohol-Related Disease Impact Applicationwhich is maintained by the Centers for Disease Control and Prevention (CDC). According to the CDC, this application “provides national and state estimates of alcohol-related health impacts, including deaths and years of potential life lost.”

The difference of age

The analysis showed that the level of an individual’s alcohol-related risk was heavily influenced by age.

In total, 35.8 percent of alcohol-related deaths occurred in people aged 20–49. When looking at deaths that were prevented by alcohol consumption, the scientists found only 4.5 percent in this age group.

When they looked at individuals aged 65 or over, it was a different story: Although a similar 35 percent of alcohol-related deaths occurred in this group, the authors found a huge 80 percent of the deaths prevented by alcohol in this demographic.

The researchers also saw this stark difference between age groups when they looked at the number of potential years lost to alcohol.

They showed that 58.4 percent of the total number of years lost occurred in those aged 20–49. However, this age group only accounted for 14.5 percent of the years of life saved by drinking.

Conversely, the over-65 group accounted for 15 percent of the overall years of life lost, but 50 percent of the years of life saved.

The authors conclude that younger people “are more likely to die from alcohol consumption than they are to die from a lack of drinking,” but older people are more likely to experience the health benefits of moderate drinking.

Although the conclusions are not explosive, they bring us a more complete understanding of alcohol’s impact on health: Moderate drinking may benefit people of a certain age group, but heavy drinking is harmful to all.

iTHRIV and community groups partner to address health needs across Virginia

Four biomedical research projects to improve the health of Virginians will be funded by the integrated Translational Health Research Institute of Virginia (iTHRIV), a Clinical Translational Science Award Hub.

“iTHRIV is excited to partner with the National Institutes of Health in supporting our community nonprofit and governmental organizations who are collaborating with academic researchers to address important health needs across Virginia,” said University of Virginia Associate VP for Clinical & Translational Research and Director of iTHRIV Karen Johnston. “It is our hope that these pilot grant projects will benefit underserved communities and improve research partnerships.”

The projects address autism spectrum disorder, improved access to colorectal cancer (CRC) screening, postpartum depression, and the benefits of walking in cities. Community organizations will be involved in the efforts, working with teams of physicians and researchers from the University of Virginia and Virginia Tech.

Our unique approach to community engagement through regional iTHRIV advisory boards in northern, central, and southwest/southside Virginia ensures that we foster collaborative research among community, clinical and academic organizations and institutions to serve diverse communities across the majority of the Commonwealth. The opportunity to involve our community partners in research that is a priority for them is extremely rewarding.”

Kathy Hosig, Associate Professor & Director, Center for Public Health Practice and Research, Virginia Tech

The four teams will be awarded a total of $80,000 in funding.

Improving access to care for autism spectrum disorder in rural southwest Virginia

Disparities exist in access to care for parents and their children affected by autism spectrum disorder (ASD) in rural communities. The iTHRIV seed grant funding will address barriers to accessing ASD specialty services in southwest Virginia, including diagnostic assessments and case management. The partnership between K.J. Holbrook from the Mount Rogers Community Services Board and Angela Scarpa, a professor of psychology at Virginia Tech, will provide information on the best ways to provide education and support for underserved communities about ASD care.

The impact of urban walking on public health

Based on the 2017 Community Health Assessment undertaken in Richmond, Va., there is a need to improve city-wide physical activity by increasing walking. It is important to understand the optimal conditions for these walks, taking into account the benefits of some spaces over others on personal outcomes such as mood and cognition and environmental outcomes such as air quality and temperature. Led by Jeremy Hoffman from the Science Museum of Virginia, Jenny Roe Director of the Center for Design and Health at the University of Virginia, Chris Neale from the University of Virginia Frank Batten School of Public Policy, and Julia Gohlke, an associate professor of population health sciences at Virginia Tech, this research will help address the issue of understanding the benefits of walking in cities.

Improving effectiveness of colorectal cancer screening through a community health center partnership

Rural and socioeconomically disadvantaged groups have lower colorectal cancer screening rates and higher mortality rates. Community health centers are ideal organizations to improve colorectal cancer screening for these groups. This research, led by Michelle Brauns from the Community Health Center of the New River Valley and Jamie Zoellner from the University of Virginia Department of Public Health Sciences, seeks to develop sustainable cancer prevention and detection programs in the New River Valley and test a scalable and low-cost CRC screening intervention.

Addressing postpartum depression and other mood and anxiety disorders in childbearing women in Charlottesville

Postpartum depression (PPD) and other perinatal mood and anxiety disorders (PMADs) are the most common complications of pregnancy and childbirth, affecting 1 in 5 mothers. At least 700 women in Greater Charlottesville will experience PMADs each year, affecting an additional 2,400 family members. Untreated PMADs can have long-term impact on the mother, baby and society. The project team, led by Adrienne Griffen from Postpartum Support Virginia and Sharon Veith from the University of Virginia School of Nursing, has the goal of educating local stakeholders about PMADs, establishing additional resources for recovery and ensuring that all childbearing women are educated about, screened for and receive treatment for PMADs from conception through one year after giving birth.

Autism Signs and Symptoms

What Is Autism?
Autism is a brain disorder that limits a person’s ability to communicate and relate to other people. It first appears in young children, who fall along a spectrum from mild to severe. Some people can navigate their world, some have exceptional abilities, while others struggle to speak. Autism spectrum disorders (ASDs) affect about one child in 88, striking nearly five times as many boys as girls.


Signs of Autism

Before a child turns three, careful observers can see signs of autism. Some children develop normally until 18-24 months old and then stop or lose skills. Signs of an ASD can include:

  • Repeated motions (rocking or spinning)
  • Avoiding eye contact or physical touch
  • Delays in learning to talk
  • Repeating words or phrases (echolalia)
  • Getting upset by minor changes

It’s important to note that these signs can occur in children without ASDs, too.

Early Warning Signs: First Year

Even young infants are very social, so it’s possible to detect signs of autism in how babies interact with their world. At this age, a child with an ASD may:

  • Not turn to a mother’s voice
  • Not respond to his own name
  • Not look people in the eye
  • Have no babbling or pointing by age one
  • Not smile or respond to social cues from others

Babies who do not have autism can have these behaviors, too, but it’s best to contact your doctor right away with any concerns.

 

Other Signs and Symptoms

People with autism sometimes may have physical symptoms, including digestive problems such as constipation and sleep problems. Children may have poor coordination of the large muscles used for running and climbing, or the smaller muscles of the hand. About a third of people with autism also often have seizures.

Early Warning Signs: Year Two

The signs of autism are more noticeable in a child’s second year. While other children are forming their first words and pointing to things they want, a child with autism remains detached. Signs of autism include:

  • No single words by 16 months
  • No pretend games by 18 months
  • No two-word phrases by age 2
  • Loss of language skills
  • No interest when adults point out objects, such as a plane flying overhead

Autism Estimates in U.S.A

One in 68 American children is now diagnosed with autism or a related disorder, federal health officials reported Thursday.

That’s a 30 percent increase from just two years ago when the estimate was one in 88 children, according to a new report from the U.S. Centers for Disease Control and Prevention.

“The number of children identified with autism continues to rise,” said Coleen Boyle, director of the CDC’s National Center on Birth Defects and Developmental Disabilities.

The continuing increase in the percentage of kids diagnosed with autism could be due to better detection of the developmental disorder, Boyle said, but also might reflect an actual increase in autism.

“It could be a combination of better recognition and increased prevalence,” she said. “Our system tells us what’s going on. It only gives us clues about the why.”

The new statistics also continue to show that autism spectrum disorder is five times more common among boys than girls. And they reflect an increase in the percentage of children being diagnosed with high-functioning autism, the CDC said.

People with an autism spectrum disorder display impaired social and communication skills. Symptoms, which can range from mild to severe, usually become apparent in the first three years of life. The developmental disorder is linked to abnormal biology and chemistry in the brain, according to the U.S. National Institutes of Health.

The CDC bases its estimates on reports from 11 communities that participate in its Autism and Developmental Disabilities Monitoring Network. The newest estimate is based on data from 2010.

Estimates of autism among 8-year-olds have more than doubled since the CDC network’s first report in 2007, which calculated that about 1 in 150 children had the disorder based on 2002 data.

The continuing rise of autism highlights the need for more funding for research into the causes of autism and for support and treatment of kids diagnosed with the disorder, said Michael Rosanoff, associate director of research and scientific review at Autism Speaks.

“We really need to double down on our research into the environmental factors that work in some complex way with a child’s genetics to increase the risk of autism,” he said.

There also needs to be continued emphasis on earlier diagnosis of autism, added Dr. Melissa Nishawala, an assistant professor of child and adolescent psychiatry at the NYU School of Medicine and medical director of the Autism Spectrum Disorders Clinical and Research Program.

The new CDC study reports that most children are diagnosed with autism spectrum disorder after age 4, even though autism can be diagnosed as early as age 2.

“We need to push the frontier of diagnosis down to the earliest ages we can,” Nishawala said. “The earlier we intervene, the more we can do to help nudge those brain pathways closer and closer to normal.”

SELMA BLAIR FINISHES INTENSE ROUND OF MS TREATMENT

Islam Magdi | around 12 hours back

| around 12 hours back

LONDON – Selma Blair has completed an exceptional round of treatment for her various sclerosis.

The 47-year-old entertainer has been open about her battles with MS since she was determined to have the condition a year ago, and in another Instagram post transferred on Thursday – a similar day as her eight-year-old child Arthur’s birthday – she has uncovered she’s been released from the consideration of a “mind blowing group of attendants” following her most recent round of treatment.

https://www.instagram.com/p/B0WCYC6HOyp/?utm_source=ig_embed

Posting an image of herself close by her Alinker walk help bicycle – in which she likewise appeared her newly shaved head – she expressed: “Today is a standard day. I am being released from the consideration of a mind boggling group of attendants and specialists and a visionary Dr. who puts stock in my recuperating as much as I do. This has been a procedure. What’s more, will keep on being one. I am immunocompromised for next a quarter of a year in any event. So no kisses please. I needed to ensure any difficulties that may emerge here were my private space. What’s more, we traversed splendidly.

“I thank all of you for your adoration and support and that additional portion of extraordinary with a @people spread. I see things a great deal more obviously now. What’s more, I am eager to share this adventure when I am prepared. For the time being, I have recuperation. What’s more, an incredible @thealinkerworld so I gotta split. Bye!!!!!! This is the best blessing I could provide for Arthur. #newimmunesystem#whodis? (sic)”

In spite of effectively completing her treatment, the Cruel Intentions star as of late said she’s “apparently more wiped out”.

Composing on Instagram not long ago, she stated: “After I conceived an offspring and felt half dead constantly, after the wrath and the tears, after my heart detonated with minding and comprehension, before any finding, I looked for this steed. I knew the main spot I was truly developing with self esteem was at @cellardoorequestrian. My coach discovered me #skytop. He should have been ready to deal with kisses. Essential. Genuinely. Also, he did. #mrnibbles. We just had a brief span before I couldn’t get to him or remain on. Yet, he has made significant progress. Also, despite the fact that I may appear as though I have gone more distant away, I am learning and getting more advantageous. Indeed, even as I get apparently more debilitated. I will hop this pony around once more. Bearing horseshows will require some real work open doors ahead. So I am requesting everything. I am inquiring. For us all who need it. Inquire. Inquire. Tune in. I have the unicorn. Presently I must almost certainly discover him once more. #tbt. #loveheals (sic)”

What’s more, the entertainer recently uncovered she “can’t envision feeling OK once more”.

She conceded: “Here’s a reality. I feel debilitated as all hellfire. I am retching and every one of the things which are not obliging to discuss. My child fled. From me. I need to get him to class. The restorative medications cause significant damage. I will get past this. We do. This will pass. Also, to mothers and fathers who watch their children wiped out on things we take to show signs of improvement… I hold you. So happy this is me and not my tyke. I can’t envision consistently feeling alright once more. #roughday. We overcome. #realitycheck (sic)”

See if you’re eligible, how to file a claim and see how much you’ll get

If you were among the 147 million people whose data was exposed in the major Equifax data breach in 2017, you now see if you are eligible to submit a claim and then file one to recover money you spent or lost as a result of the hack. The Federal Trade Commission said this week that Equifax has agreed to pay at least $575 million and up to $700 million to help compensate victims of hackers who stole personal data from Equifax servers. Payments as part of the settlement can cover the costs to recover from the security breach of the free credit report company — including recovering from the theft of your identity — and unauthorized charges to your account. You can also submit a claim to cover the cost of protecting yourself from identity theft, following the Equifax data breach. And even if you weren’t part of the breach and don’t file a claim, you can get free credit reports for seven years. The breach resulted in hackers stealing Social Security numbers, addresses, credit card and driver’s license information, birthdates and other personal data stored on Equifax’s servers. As part of its investigation, the FTC alleged that the free credit bureau failed to take reasonable steps to secure its network.Taking part in the Equifax settlement isn’t completely straightforward. To get started, you can check if you and your information were exposed as part of the breach. Then, if you were, gather documents related to the hack that show your expenses and losses. And finally, submit your claim for compensation. You have until January 22, 2020 to file. READ MORE Equifax to pay at least $575M as part of FTC settlement Former Equifax exec gets 4 months in prison for insider trading after breach Thanks to Equifax breach, 4 US agencies don’t properly verify your data, GAO finds The exact amount that Equifax will pay out is undetermined. The proposed settlement will start with a $300 million fund to compensate affected consumers who bought credit-monitoring services. Equifax will also pay $175 million to state and districts — and $100 million to the Consumer Financial Protection Bureau in civil penalties. If the initial $300 million infusion doesn’t adequately compensate consumers, according to the FTC, Equifax has agreed to kick in $125 million more to the fund, for a total possible settlement payout of $700 million. If you’re a claimant, your share of the settlement could include free credit-monitoring and identity-theft protection services. You might also be eligible for cash payments to cover expenses as a result of the breach — such as legal fees and credit monitoring — free help recovering from identity theft and free credit reports for 10 years.