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People cannot donate their blood if they are high risk for Mad Cow Disease variant

People cannot donate their blood if they are high risk for variant Creutzfeld-Jacobs Disease (vCJD), thought to be the human form of Mad Cow Disease. Why are so many Americans considered high risk,…

Source: People cannot donate their blood if they are high risk for Mad Cow Disease variant

People cannot donate their blood if they are high risk for Mad Cow Disease variant

People cannot donate their blood if they are high risk for variant Creutzfeld-Jacobs Disease (vCJD), thought to be the human form of Mad Cow Disease.

Why are so many Americans considered high risk, and will we ever be able to give blood? After looking into those questions, I realized just how tricky they are.

From 1986–98, the UK saw an epidemic of bovine spongiform encephalopathy (BSE), a neurodegenerative disease in cattle likely caused by unsafe feeding practices. By ’96 the disease appeared to have crossed to humans, as scientists identified the first case of vCJD and strongly linked it to BSE.

The human form was fatal and incurable: as of May 2015, it had killed at least 228 people, including 177 in the UK and 27 in France. Scientists suspect that vCJD may also be transmissible through human donations of blood, organs, and tissue, based on animal studies and several cases where humans were diagnosed with the disease after a transfusion.

While human cases have declined sharply since 2000, the disease can theoretically incubate for decades, and experts have warned that a second wave could break out. Until recently, it was impossible to test for.

Who is at risk of vCJD? Theoretically, anyone who has consumed cattle products or received a blood or organ donation has at least some risk (likely very low), as (1) we have no perfect way of containing cattle products from infected areas and (2) any cow could spontaneously get BSE, though it’s rare, and (3) we have no perfect way of preventing blood, organ, and tissue transmission. But people who lived near the center of the epidemic may face much higher risk.

The Food and Drug Administration has spent the past 20 years trying to figure out the right mix of people to keep out of the blood pool. According to a 2015 report, its vCJD recommendations keep away an estimated 254,000 annual donors. Given that less than 10% of eligible donors give blood each year, we can safely assume that the number of Americans blocked because of vCJD risk therefore is in the millions.

But history shows that this group is pretty haphazard.

In 1999, the FDA recommended deferring anyone who had spent six months in the UK from 1980 to 1996 (when the UK implemented extensive controls to contain BSE).

In 2001, it expanded deferrals to include anyone who

—spent five years in any European country but the UK between 1980 and the present

—spent three months in the UK from 1980 through the end of 1996

—spent six months in Europe on a US military base from 1980 through the end of 1996

—received a blood transfusion in the UK from 1980 to present

Around that time, the FDA warned that the new policy would have turned away 5% of potential donors, or around 508,000 people, for a 90% reduction of vCJD blood transmission risk relative to how things were before the 1999 recommendations.

But experts continued to recommend changes one way or another.

In 2006, an FDA committee decided in a close vote not to recommend deferring French transfusion patients. In 2006, however, the FDA added them to the list anyway.

In 2011, after several vCJD cases were identified among people from Saudi Arabia, an FDA committee voted to defer people who had spent 5 years there since 1980. The FDA, however, chose to wait for a broader reevaluation of policy.

In 2015, an FDA committee considered clearing people who had spent time in European countries other than the UK, France, and Ireland. The proposal didn’t go through, with some members complaining about the risk model used or inconsistencies in how countries were treated.

Meanwhile, researchers found that a US man had died in 2014 of vCJD that he likely picked up while living in Kuwait, Russia, or Lebanon — countries not even on the FDA’s deferral list.

Some countries, of course, can’t afford to be as stringent as the US. Notably, the UK blocks blood transfusions only from locals who have themselves received donations or been diagnosed with vCJD, while also sourcing internationally for some blood products.

Ultimately, we’re waiting on science to end to the vCJD crisis, and there has been some meaningful progress there. Blood transfusions increasingly use leukoreduction, or the removal of white blood cells, which appears to limit risk of vCJD transmission and could be a step toward blocking it. Scientists have developed a vCJD test and are studying how it could be implemented. Scientists are also researching cures for prion diseases like vCJD.

We’re also waiting on studies in the UK and elsewhere to see just how widespread vCJD is and whether it might just fade away.

Two people with unalike HLA, can produce a baby with super-charged immune system

The human leukocyte antigen (HLA) system is a gene complex encoding the major histocompatibility complex (MHC) proteins in humans. These cell-surface proteins are responsible for the regulation of …

Source: Two people with unalike HLA, can produce a baby with super-charged immune system

Two people with unalike HLA, can produce a baby with super-charged immune system

The human leukocyte antigen (HLA) system is a gene complex encoding the major histocompatibility complex (MHC) proteins in humans. These cell-surface proteins are responsible for the regulation of the immune system in humans. The HLA gene complex resides on a 3 Mbp stretch within chromosome 6p21. HLA genes are highly polymorphic, which means that they have many different alleles, allowing them to fine-tune the adaptive immune system. The proteins encoded by certain genes are also known as antigens, as a result of their historic discovery as factors in organ transplants. Different classes have different functions:

HLAs corresponding to MHC class I (A, B, and C) present peptides from inside the cell. For example, if the cell is infected by a virus, the HLA system brings fragments of the virus to the surface of the cell so that the cell can be destroyed by the immune system. These peptides are produced from digested proteins that are broken down in the proteasomes. In general, these particular peptides are small polymers, about 9 amino acids in length.[citation needed] Foreign antigens presented by MHC class I attract killer T-cells (also called CD8 positive- or cytotoxic T-cells) that destroy cells. MHC class I proteins associate with β2-microglobulin, which unlike the HLA proteins is encoded by a gene on chromosome 15.

HLAs corresponding to MHC class II (DP, DM, DOA, DOB, DQ, and DR) present antigens from outside of the cell to T-lymphocytes. These particular antigens stimulate the multiplication of T-helper cells, which in turn stimulate antibody-producing B-cells to produce antibodies to that specific antigen. Self-antigens are suppressed by regulatory T cells.

HLAs corresponding to MHC class III encode components of the complement system.

HLAs have other roles. They are important in disease defense. They are the major cause of organ transplant rejections. They may protect against or fail to protect (if down-regulated by an infection) against cancers.[1] Mutations in HLA may be linked toautoimmune disease (examples: type I diabetes, coeliac disease). HLA may also be related to people’s perception of the odor of other people, and may be involved in mate selection, as at least one study found a lower-than-expected rate of HLA similarity between spouses in an isolated community.[2]

Aside from the genes encoding the 6 major antigen-presenting proteins, there is a large number of other genes, many involved in immune function, located on the HLA complex. Diversity of HLAs in the human population is one aspect of disease defense, and, as a result, the chance of two unrelated individuals with identical HLA molecules on all loci is very low. HLA genes have historically been identified as a result of the ability to successfully transplant organs between HLA-similar individuals.

Source: Wiki


The researchers found that if two animals with unalike major histocompatibility complexes (or MHC) — which is what scientists call all animals’ version of HLA — loved each other very much and they mixed their bodily fluids together, then their baby would be born with a super-charged immune system.

http://www.redbookmag.com/love-sex/relationships/news/a46033/how-your-body-finds-the-one-according-to-science/

Psyllium fiber delays sugar absorption

How can I get psyllium?

Psyllium is most commonly consumed in powder or wafer form. It is also available in capsules, granules, and in liquid form. It is the main ingredient in many over-the-counter laxatives, including:

  • Metamucil
  • Fiberall
  • Cilium
  • Maalox Daily Fiber Therapy
  • Uni-Laxative

Follow the directions on packaging, and remember that a key component of psyllium’s work in your lower intestine is its ability to soak up liquid, so make sure to drink plenty of water daily.


Psyllium herb is like a bathroom buddy. Fibers in it encapsulates the fat and sugar out of your body. It delays sugar absorption.Sugar is food for cancer cells and viruses.

Polio virus

The term “poliomyelitis” is used to identify the disease caused by any of the three serotypes of poliovirus. Two basic patterns of polio infection are described: a minor illness which does not involve the central nervous system (CNS), sometimes called abortive poliomyelitis, and a major illness involving the CNS, which may be paralytic or nonparalytic.[12]In most people with a normal immune system, a poliovirus infection is asymptomatic. Rarely, the infection produces minor symptoms; these may include upper respiratory tract infection (sore throat and fever), gastrointestinal disturbances (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhea), and influenza-like illness.[1]

The virus enters the central nervous system in about 1% of infections. Most patients with CNS involvement develop nonparalytic aseptic meningitis, with symptoms of headache, neck, back, abdominal and extremity pain, fever, vomiting,lethargy, and irritability.[13][14] About one to five in 1000 cases progress to paralytic disease, in which the muscles become weak, floppy and poorly controlled, and, finally, completely paralyzed; this condition is known as acute flaccid paralysis.[15] Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal.Encephalitis, an infection of the brain tissue itself, can occur in rare cases, and is usually restricted to infants. It is characterized by confusion, changes in mental status, headaches, fever, and, less commonly, seizures and spastic paralysis.[16]

Cause

Main article: Poliovirus

A TEM micrograph of poliovirus

Poliomyelitis is caused by infection with a member of the genus Enterovirus known as poliovirus (PV). This group of RNA viruses colonize the gastrointestinal tract[17] — specifically the oropharynx and the intestine. The incubation time (to the first signs and symptoms) ranges from three to 35 days, with a more common span of six to 20 days.[1] PV infects and causes disease in humans alone.[18] Its structure is very simple, composed of a single (+) sense RNA genome enclosed in a protein shell called a capsid.[18] In addition to protecting the virus’s genetic material, the capsid proteins enable poliovirus to infect certain types of cells. Three serotypes of poliovirus have been identified—poliovirus type 1 (PV1), type 2 (PV2), and type 3 (PV3)—each with a slightly different capsid protein.[19] All three are extremely virulent and produce the same disease symptoms.[18] PV1 is the most commonly encountered form, and the one most closely associated with paralysis.[20]

Individuals who are exposed to the virus, either through infection or by immunization with polio vaccine, develop immunity. In immune individuals, IgA antibodies against poliovirus are present in the tonsils and gastrointestinal tract, and are able to block virus replication; IgG and IgM antibodies against PV can prevent the spread of the virus to motor neurons of the central nervous system.[21] Infection or vaccination with one serotype of poliovirus does not provide immunity against the other serotypes, and full immunity requires exposure to each serotype.[21]

A rare condition with a similar presentation, nonpoliovirus poliomyelitis, may result from infections with nonpoliovirusenteroviruses.[22]

Source: Wiki

 


Treatment

  • General: There is no cure for polio. The goal of treatment is to control symptoms and to prevent complications. Some forms of polio require no treatment. However, severe forms may require orthopedic surgery. Common treatments include physical therapy, braces, and corrective shoes. Antiviral drugs are being studied for effectiveness against poliovirus; however, further research in this area is needed.
  • Antibiotics: Antibiotics are not effective against the polio virus itself but may be prescribed in patients that have coexisting infections, such as a urinary tract infection.
  • Bethanechol: Bethanechol may be used in polio patients who experience urinary retention.
  • Braces or corrective shoes: In cases of paralytic polio, leg braces and corrective shoes may be used to assist in proper walking. Patients who wear braces should also participate in physical therapy to prevent muscle damage associated with a lack of use.
  • Lifestyle changes: Bed rest may be advised for patients with severe forms of polio.
  • Moist heat: The use of heating pads and warm towels may be advised in patients with polio who experience muscle pain and spasms.
  • Nutritional changes: A nutritious diet is critical for patients with polio, to give the body all the resources that it needs to fight off the infection.
  • Painkillers: Painkillers may be given to manage symptoms, including headache, muscle pain, and muscle spasms. Narcotics are usually avoided due to an increased risk of breathing difficulties.
  • Physical therapy: Patients with paralytic polio may benefit from moderate exercise to prevent deformity and loss of muscle function. Swimming may benefit patients who experience pain and muscle weakness.
  • Portable ventilators: Jacket-type negative-pressure ventilators worn over the chest and abdomen assist patients with polio who are not able to breathe unassisted. In some cases, ventilator use may be temporary, although some patients may need to use them for the rest of their lives.
  • Surgery: In severe polio cases, orthopedic surgery may be performed to help recover muscle strength and function.
  • Treatments for post-polio syndrome: Post-polio syndrome may occur decades after a polio infection has run its course. Treatments available for patients with post-polio syndrome include pyridostigmine, immunoglobulin, coenzyme Q10, and physical therapy.

http://www.akins.com/ns/DisplayMonograph.asp?StoreID=A59A6B1C10E44C9E9420A7A75B27460A&DocID=condition-polio

 

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Federal programs providing direct services to caregivers of older adults in the USA

– the NFCSP; •the VA Caregiver Support Program; • FMLA; • state and local paid sick leave statutes; • various provisions in the Patient Protection and Affordable Care Act related to caregiver…

Source: Federal programs providing direct services to caregivers of older adults in the USA

Federal programs providing direct services to caregivers of older adults in the USA

– the NFCSP;
•the VA Caregiver Support Program;
• FMLA;
• state and local paid sick leave statutes;
• various provisions in the Patient Protection and Affordable Care Act related to caregivers’
role as decision makers, caregiver assessment, quality metrics, and testing of new care
models that promote person- and family-centered care;
• Medicaid’s consumer-directed options for home- and community-based services (e.g., Cash
and Counseling);
• state-funded caregiver support programs;
• the Caregiver Advise, Record, Enable (CARE) Act;
• the Lifespan Respite Act;
• Medicare hospice benefits that provide interventions for both the person and the family; and
• the National Alzheimer’s Project Act (NAPA)


Connie’s comments: Families take care of their older adults. Most of the time, they use their own money with no government assistance.

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By 2030, 72.8 million—more than one in five U.S. residents—will be age 65 or older

Family caregiving affects millions of Americans every day, in all walks of life. At least 17.7 million individuals in the United States are family caregivers of someone age 65 and older who needs help because of a limitation in their physical, mental, or cognitive functioning. As a society, we have always depended on family caregivers to provide the lion’s share of long-term services and supports (LTSS) for our elders. Yet the need to recognize and support caregivers is among the most significant overlooked challenges facing the aging U.S. population, their families, and society.

For decades, demographers, gerontologists, health researchers, health care professionals, economists and other experts have called attention to the nation’s rapidly aging population. However, little action has been taken to prepare the health care and LTSS systems for this unprecedented demographic shift. By 2030, 72.8 million—more than one in five U.S. residents—will be age 65 or older.

The greatest growth will be in the numbers of the “oldest old,” the population that is most in need of help because they are the most likely to have physical, cognitive, and other functional limitations. The increasing diversity of older Americans may further increase the demand for caregivers because data indicate that older African-American and Hispanic adults have been more likely than white adults to have functional impairments.

In less than 15 years, nearly 3 in 10 older Americans will identify as a member of a minority group. Differences in culture, along with differences in income, education, neighborhood environments, lifetime access to health care, and occupational hazards will have a significant impact on the need for care, the availability and willingness of family caregivers to provide it, and the most effective and appropriate ways to provide caregiver support.

Developing programs and services that are accessible, affordable, and tailored to the needs of diverse communities of caregivers presents significant challenges. While the need for caregiving is rapidly increasing, the pool of potential family caregivers is shrinking. Families have fewer children, older adults are more likely to have never married or to be divorced, and adult children often live far from their parents or may be caring for more than one older adult or their own children.

In the past, families could rely on women to provide what is often referred to as eldercare, especially daughters, daughters-in-law, and wives who were not in the workforce. Today, the typical caregiver is still female. But that caregiver is almost as likely as a male caregiver to be employed, to need employment income, and to have limited schedule flexibility to juggle caregiving, work, and other responsibilities.

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https://www.nap.edu/download/23606

Do immigrants take jobs from Americans and lower their wages by working for less?

Do immigrants take jobs from Americans and lower their wages by working for less? The answer, according to a report published on Wednesday by the National Academies of Sciences, Engineering and Med…

Source: Do immigrants take jobs from Americans and lower their wages by working for less?