tissue-damage

So in trend of #dontbeafruit, this is what a lucky stupid person gets. Really anon that I saw saying bones are stronger than fruit etc? In my naive state of invincibility, just sitting on a perfectly calm horse until he spooked bc of a dog. He took off bucking, just a handful of mane and I sat 3 before I tumbled to the ground in a heap. His hoof hit my arm I had been holding on with through the air, this is not being stepped on. My tissue is still damaged even today with a slightly darker patch of skin where the main abrasion was, and this was just a few hours afterwards. So even though nothing was broken, it hurt bad enough I thought I had broken it. I also had an apple sized bruise on my inner arm by my armpit where he had nicked it also. Let’s not forget the hand holding the mane had stupidly held on and dragged me a bit where I grass scratches up and down my legs. So guys, please trust and bond with your horse but don’t prove it with overly ridiculous stunts.

Itchy Wool Sweaters Explained

Johns Hopkins researchers have uncovered strong evidence that mice have a specific set of nerve cells that signal itch but not pain, a finding that may settle a decades-long debate about these sensations, and, if confirmed in humans, help in developing treatments for chronic itch, including itch caused by life-saving medications.

At the heart of their discovery is a type of sensory nerve cell whose endings receive information from the skin and relay it to other nerves in the spinal cord, which then coordinates a response to the stimulus. Published online Dec. 23 in Nature Neuroscience, a report on the research suggests that even when the itch-specific nerve cells receive stimuli that are normally pain-inducing, the message they send isn’t “That hurts!” but rather “That itches!”

Pain and itch are both important sensations that help organisms survive. And pain is arguably more important because it tells us to withdraw the pained body part in order to prevent tissue damage. But itch also warns us of the presence of irritants, as in an allergic reaction. However, “when either of these sensations continues for weeks or months, they are no longer helpful. We even see patients stop taking life-saving medications because they cause such horrible itchiness all over,” says Xinzhong Dong, Ph.D., a Howard Hughes early career scientist and associate professor of neuroscience at the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine. “And sometimes when we try to suppress chronic pain, with morphine for example, we end up causing chronic itchiness. So the two sensations are somehow related, and this study has begun to untangle them,” he says.

Because nerve cells send their messages as electrical currents that flow through them just as they would through wires, scientists can plug tiny monitors into individual nerve cells to detect the moment of stimulation. The scientific controversy over pain and itch centers around a group of nerve cells known to respond electrically to painful stimuli such as molecules of capsaicin, the fiery ingredient in chili peppers. A small subset of these nerve cells also responds electrically to itchy stimuli because they have on their surfaces receptors for molecules like histamine. One of these itchy receptors, called MrgA3, binds the anti-malaria drug chloroquine, causing serious itchiness in many patients.

Sensory nerve scientists have not known whether the nerves with itchy receptors and pain receptors were actually sending both types of messages to the brain, or just itch messages. What the current study found is that, in nerves with the itchy receptor MrgA3, electrical signals sent in response to both painful and itchy stimuli are interpreted by the brain as itch.

To reach this conclusion, the researchers first used a genetic trick to label the MrgA3 cells in mice with a glowing protein that allowed them to see the cells under the microscope. Aided by the glow, they were able to plug in those tiny electricity monitors and watch nerve cell responses to different stimuli. The cells transmitted electrical signals when the mice were exposed to itch-inducing chloroquine and histamine, as well as pain-inducing capsaicin and heat. Based on this result, the researchers tentatively concluded that the cells could send both pain and itch signals.

In the next experiment, the researchers monitored the behavioral responses of mice to the different stimuli. As expected, when the tails of normal mice were placed in hot water, they quickly pulled them out; when normal mice were given a bit of chloroquine or histamine, they scratched vigorously with their hind legs.

Then, to examine the role of MrgA3 cells in pain and itch, the scientists selectively killed MrgA3 nerve cells in adult mice and retested their responses. Presumably, the researchers noted, because MrgA3 cells are only a small fraction of all pain-sensing nerve cells, the mice had normal withdrawal responses to painful stimuli like hot water. However, when exposed to itchy stimuli, their scratching responses were reduced to varying degrees depending on the stimulus, most significantly in response to chloroquine. The fact that some stimuli still caused scratching suggested to the scientists that MrgA3 cells are not the only ones in the body that respond to itch. “We were convinced that MrgA3 cells are responsible for much of the sensation of itch, but it wasn’t yet clear whether MrgA3 cells could also relay painful information,” says Dong.

In their final experiments, the scientists used genetic techniques to create mice in which the MrgA3 cells were the only cells in the body capable of responding to capsaicin, that peppery pain-inducing substance. When injected into the cheeks of mice, normal mice massage the area with their forepaws to relieve the hot sensation. When injected into the experimental mice, they vigorously scratched their cheeks with their hind legs, suggesting that this normally painful stimulus had been communicated to the brain—by MrgA3 cells—as itchiness.

“Now that we have disentangled these itchy sensations from painful ones, we should be able to design drugs that target itch-specific nerve cells to combat chronic itchiness,” says Dong. “We hope that this will not only provide relief, but also increase people’s faithfulness to their drug plans, particularly for deadly diseases like malaria and cancer.”

Multiple sclerosis study reveals how killer T cells learn to recognize nerve fiber insulators

A micrograph of a killer T cell, a white blood cell that destroys germs or cancers, but that can sometimes attack the body’s own normal cells.

Misguided killer T cells may be the missing link in sustained tissue damage in the brains and spines of people with multiple sclerosis, findings from the University of Washington reveal. Cytoxic T cells, also known as CD8+ T cells, are white blood cells that normally are in the body’s arsenal to fight disease.

Multiple sclerosis is characterized by inflamed lesions that damage the insulation surrounding nerve fibers and destroy the axons, electrical impulse conductors that look like long, branching projections. Affected nerves fail to transmit signals effectively.

Intriguingly, the UW study, published this week in Nature Immunology, also raises the possibility that misdirected killer T cells might at other times act protectively and not add to lesion formation. Instead they might retaliate against the cells that tried to make them mistake the wrappings around nerve endings as dangerous.

Scientists Qingyong Ji and Luca Castelli performed the research with Joan Goverman, UW professor and chair of immunology. Goverman is noted for her work on the cells involved in autoimmune disorders of the central nervous system and on laboratory models of multiple sclerosis.

Multiple sclerosis generally first appears between ages 20 to 40. It is believed to stem from corruption of the body’s normal defense against pathogens, so that it now attacks itself. For reasons not yet known, the immune system, which wards off cancer and infection, is provoked to vandalize the myelin sheath around nerve cells. The myelin sheath resembles the coating on an electrical wire. When it frays, nerve impulses are impaired.

Depending on which nerves are harmed, vision problems, an inability to walk, or other debilitating symptoms may arise. Sometimes the lesions heal partially or temporarily, leading to a see-saw of remissions and flare ups. In other cases, nerve damage is unrelenting.

The myelin sheaths on nerve cell projections are fashioned by support cells called oligodendrocytes. Newborn’s brains contain just a few sections with myelinated nerve cells. An adult’s brains cells are not fully myelinated until age 25 to 30.

For T cells to recognize proteins from a pathogen, a myelin sheath or any source, other cells must break the desired proteins into small pieces, called peptides, and then present the peptides in a specific molecular package to the T cells. Scientists had previously determined which cells present pieces of a myelin protein to a type of T cell involved in the pathology of multiple sclerosis called a CD4+ T cell. Before the current study, no cells had yet been found that present myelin protein to CD8+ T cells.

Scientists strongly suspect that CD8+ T cells, whose job is to kill other cells, play an important role in the myelin-damage of multiple sclerosis. In experimental autoimmune encephalitis, which is a mouse model of multiple sclerosis in humans, CD4+ T cells have a significant part in the inflammatory response. However, scientists observed that, in acute and chronic multiple sclerosis lesions, CD8+T cells actually outnumber CD4+ T cells and their numbers correlate with the extent of damage to nerve cell projections. Other studies suggest the opposite: that CD8+ T cells may tone down the myelin attack.

The differing observations pointed to a conflicting role for CD8+ T cells in exacerbating or ameliorating episodes of multiple sclerosis. Still, how CD8+ T cells actually contributed to regulating the autoimmune response in the central nervous system, for better or worse, was poorly understood.

TIP dendritic cells, stained to show their physical features.

Goverman and her team showed for the first time that naive CD8+ T cells were activated and turned into myelin-recognizing cells by special cells called Tip-dendritic cells. These cells are derived from a type of inflammatory white blood cell that accumulates in the brain and the spinal cord during experimental autoimmune encephalitis originally mediated by CD4+ T cells. The membrane folds and protrusions of mature dendritic cells often look like branched tentacles or cupped petals well-suited to probing the surroundings.

The researchers proposed that the Tip dendritic cells can not only engulf myelin debris or dead oligodendrocytes and then present myelin peptides to CD4+ T cells, they also have the unusual ability to load a myelin peptide onto a specific type of molecule that also presents it to CD8+ T cells. In this way, the Tip dendritic cells can spread the immune response from CD4+ T cells to CD8+ T cells. This presentation enables CD8+ T cells to recognize myelin protein segments from oligodendrocytes, the cells that form the myelin sheath. The phenomenon establishes a second-wave of autoimmune reactivity in which the CD8+ T cells respond to the presence of oligodendrocytes by splitting them open and spilling their contents.

“Our findings are consistent,” the researchers said, “with the critical role of dendritic cells in promoting inflammation in autoimmune diseases of the central nervous system.” They mentioned that mature dendritic cells might possibly wait in the blood vessels of normal brain tissue to activate T-cells that have infiltrated the blood/brain barrier.

The oligodendrocytes, under the inflammatory situation of experimental autoimmune encephalitis, also present peptides that elicit an immune response from CD8+ T cells. Under healthy conditions, oligodendrocytes wouldn’t do this.

The researchers proposed that myelin-specific CD8+ T cells might play a role in the ongoing destruction of nerve-cell endings in “slow burning” multiple sclerosis lesions. A drop in inflammation accompanied by an increased degeneration of axons (electrical impulse-conducting structures) coincides with multiple sclerosis leaving the relapsing-remitting stage of disease and entering a more progressive state.

Medical scientists are studying the roles of a variety of immune cells in multiple sclerosis in the hopes of discovering pathways that could be therapeutic targets to prevent or control the disease, or to find ways to harness the body’s own protective mechanisms. This could lead to highly specific treatments that might avoid the unpleasant or dangerous side effects of generalized immunosuppressants like corticosteroids or methotrexate.

anonymous asked:

I have to go to the doctors for a suspected connective tissue disease, I'm glad to finally be getting somewhere. If I have a diagnosis people can't make me feel crazy, by saying it's in my head. I just have a feeling my life is about to change drastically and turn into a whirlwind of doctors and specialists and it's so nerve-racking. Any advice?

Hi Hi,

Being diagnosed with something can be very scary, no joke. I’ve been diagnosed with a ton of things (depression, anxiety, eating disorder etc) and you know what? It made me feel a lot better knowing that I had these things & knowing that I’ll be okay and I’ll have a great support system.

People are going to talk, people are going to say that “its just in your head” but do they know what you’re really going though? No. Of course not. They are not you, you are you, you are the only person who really knows how you’re feeling & what’s going on inside your head- along with your mental health etc.

Your life is going to change no matter what you do, It’s just life. Being diagnosed with sometime surly isn’t the end of the world, most of the time it’s a new beginning because then you know some more about yourself, you can understand yourself some more and so on forward.

My best advice for you is to stay calm and remember that being diagnosed with something doesn’t make you any less of a person nor any different. You’re still you and you’re still the best you can be. <3

Is Copd Hereditary



Is COPD Hereditary?

Chronic obstructive pulmonary disease, or COPD, is a serious chronic condition that leads to progressively reduced lung capacity because of persistent inflammation and tissue damage. While normally seen in smokers, people who lack the enzyme Alpha1-antitrypsin (AAT) are at increased risk for developing the disease.

History

COPD is first described in medical literature in the 19th century. British physician Charles Badham and French physician Rene Laennec (inventor of the stethoscope) both described it as chronic bronchitis and emphysema. By the 1860s, the common progression of the disease–chronic bronchitis with repeated infections, ending in heart failure–was included in British medical textbooks. It was more prevalent among the poor, likely because of their exposure toxins, and thus was attributed to bad living.

Identification

COPD, as the name suggests, is a state of chronic airway obstruction in the lungs due to either bronchitis, emphysema or both. The obstruction is usually progressive but in some cases is partially reversible. Symptoms include a long-term, productive cough, wheezing and breathlessness. Physical examinations and pulmonary tests followed by a chest radiograph or CT scan are used to make a diagnosis. If the patient is under 40 or has a family history of early COPD, genetic testing is often performed to check for AAT deficiency.

Types

Chronic bronchitis is indicated by the presence of a a productive (mucus-producing) cough, attributable only to bronchitis, for 3 months per year for at least 2 consecutive years. Bronchitis causes mucus gland enlargment, inflammation and the thickening of the bronchial wall. Airway walls can narrow and become deformed; supporting tissue can be lost as well.

Emphysema is the permanent enlargment of air spaces around the bronchial tubes and the destruction of the bronchial walls. Emphysema may occur primarily around the bronchials or around the alveolus, (behind the bronchials, where gas exchanges in the blood take place). This second type of emphysema is commonly seen in patients with AAT deficiency.

For most COPD patients, the airway inflammation seen in bronchitis and the tissue destruction seen in emphysema are both present. The inflammation can be treated and sometimes reversed, but the tissue damage cannot.

Considerations

The major cause of COPD is cigarette smoking, developing in 15 percent of smokers and accounting for 90 percent of one’s risk for developing the disease. Other factors include secondhand smoke and air pollution.

There is one known genetic risk factor, alpha1-antitrypsin (AAT) deficiency, but it accounts for only 1 percent of COPD cases in the U.S. AAT inhibits an enzyme called neutrophil elastase, which can cause the tissue damage seen in emphysema if it is not broken down efficiently by the body. A mutated gene inherited from one parent can cause a mild deficiency, but limiting one’s exposure to smoke and pollution can generally prevent COPD. However, if two damaged genes are inherited, it is likely that the patient will develop COPD regardless of any precautions.

Prevention/Solution

Aside from those with an AAT deficiency, COPD is rarely seen in non-smokers. This is the best preventative measure one can take. If a smoker is diagnosed with COPD, the first step is always a smoking cessation plan. Other treatments include oral or inhaled steroids, bronchodilators, mucolytic agents, oxygen therapy and antibiotics to treat any lung infections, which are common in people with COPD. Patients with AAT deficiency may receive infusions of AAT harvested from donated blood plasma. Pulmonary rehabilitation is frequently recommended.

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Raphael Carl Lee

Raphael Carl Lee is  is an american surgeon, medical researcher, biomedical engineer, and entrepreneur. He was born October 29, 1949 in Sumter, South Carolina. He received his medical degree from Temple University and completed his residency at Massachusetts General Hospital in Boston. He is regularly considered one of the top plastic surgeons in America and specializes in scar tissue repair. In addition to practicing surgery, he conducts research to better understand the mechanisms of electrical shock injury and develop treatments for tissue damage. These treatments center around repairing cell membranes with synthetic compounds. If left untreated, cell membrane damage leads to the tissue damage observed in heart attacks, strokes, limb reattachment after a prolonged period and radiation injury. He currently works as a clinical investigator at the University of Chicago. 

Researchers Developing Drug That Regenerates Damaged Tissue

A joint team of researchers from Case Western Reserve and the University of Texas Southwestern have developed a drug that repairs damaged tissue and promotes regeneration in tissue stem cells. 

“We are very excited,“ said Sanford Markowitz, MD, PhD, the Ingalls Professor of Cancer Genetics at the university’s School of Medicine and a medical oncologist at University Hospitals Case Medical Center’s Seidman Cancer Center. “We have developed a drug that acts like a vitamin for tissue stem cells, stimulating their ability to repair tissues more quickly. The drug heals damage in multiple tissues, which suggests to us that it may have applications in treating many diseases.”

The next step for the team will be developing the drug and proving it’s safe to testing on larger animals and humans. The main goal for the drug is to significantly speed up the recovery process in tissue, from organs to marrow and muscle. The development of this drug could have dynamic benefits, including increasing the survival rates of those with liver cancer by allowing doctors to performs more successful surgeries on the liver.

READ FULL ARTICLE HERE 

Funding for the study came from Case Western Reserve University School of Medicine’s Council to Advance Human Health (CAHH), from the Harrington Discovery Institute at University Hospitals, and from multiple National Institutes of Health grants that included the Case GI SPORE, led by Markowitz, and the National Center for Accelerating Innovation at the Cleveland Clinic. Additional support was received from the Marguerite Wilson Foundation; the Welch Foundation; the Cancer Prevention & Research Institute of Texas; Inje University; and the Korean National Research Foundation. Generous major gifts also came from the Leonard and Joan Horvitz Foundation and the Richard Horvitz and Erica Hartman-Horvitz Foundation.

Phoenix mythology

I THINK I KNOW WHAT PARRISH IS!

After some research on Wikipedia and help from my friend famke44 I found out that Parrish could possibly be a phoenix.

Phoenix :

 “A phoenix or phenix (Greek: φοῖνιξ phoinix) is a long-lived bird that is cyclically regenerated or reborn. Associated with the sun, a phoenix obtains new life by arising from the ashes of its predecessor.”

Phoenix abilities:

Ash Resurrection : “Upon death, the user’s body turns into ash (the body may slowly turn into ash or even burst into flames until it is ash) and come out anew. It is a passive ability, so it happens the instant the user is killed.”

Regenerative Healing Factor :  “The user can rapidly regenerate, in other words, they recreate lost or damaged tissues, organs and limbs, sometimes slowing, or even stopping, aging. They are generally in very good physical shape as their bodies are constantly reverting to healthy state.”

Parrish may have died in the fire and came back to life afterwards.

Remember the scenes where Parrish brings dead bodies to the Nemeton? With all the fire surrounding him and the dead bodies? What if he’s trying to bring the dead back to life, by turning the bodies into ash so that they can ‘reborn’ with the help of the Nemetons power? Maybe he’s trying to bring people back who did not deserve to die? I have a feeling that this theory might actually be true.

SCAFFOLD

Researchers want to develop biocompatible polymers that would serve as scaffolding that helps regrow tissue, replacing damaged or missing flesh and organs in patients. A Swedish team developed the high-molecular-weight polymer shown above, which fluoresces strongly under near-infrared light, a part of the spectrum where most flesh is transparent. In lab rats, the researchers monitored the scaffolding mats with near-IR light and observed that it was colonized by rat tissue and blood vessels.

Credit: Adv. Funct. Mater. 2015, DOI: 10.1002/adfm.201500351

(Enter our photo contest here)

Related C&EN Content:

Putting Stem Cells In Their Place

Coaxing Tissue To Regenerate

Graphene That’s Fit To Print

I have been putting off this post for awhile because I am unsure how this will come across. I might just delete it later because I don’t like to babble about this stuff.
So if you are like “TL;DR” The short of it is: 

“health very bad, brain broken, blah stroke blah blah”

Keep reading

Photo credit to horseandhound.co.uk.

Splay Footed: Toes turned outwards. Creates a longer stride, which is less efficient in forward motion. Can often cause hard or soft tissue damage, if one leg is hitting off the other. This is not uncommon in foals, as they are not finished growing. Often corrects itself with growth.
Splay foot puts more pressure on the knee, causing stress or strain to ligaments, tendons and joints, as well as splints.

Pegeon Toed: Toes turned inwards. Causes horse to make a paddling motion in front steps, causing strain to tendons, joints and ligaments. Can cause a horse to develop a side bone.

Knock Kneed: Arched in at the knees. Often called crook-kneed, or in-at-the-knee. Occurs with uneven growth of legs in foals. Causes deformity in splint bones. May cause lameness problems.

Base Narrow: Close set legs, noticeable at the cannon bones. This also causes a paddling motion in the front knees. It gives the horse a narrow base and causes stress on the outside of the knee. Horses with this fault have less support of its upper body. 

Base Wide: Wide set legs, noticeable at the cannon bones. This causes stress on the inside of the knee. It takes the support away from directly under the horse. Often leads to shoulder soreness from mis-use or over-use.

So, yesterday my cousin was at Cheer camp and got elbowed right in the eye.

Ended up fracturing her eye socket in two places, her vision is very blurry with a small chance of permanent damage but not sure on that yet, along with a bit of tissue damage and she had surgery today to get a plate in to help heal the fracture.

Being the type of cousin I am, when I got to talk to her yesterday, the first thing I asked was “So should I mail you an eye patch and start calling you ‘Captain’ now?”

anonymous asked:

I've been binding for around three years now, and I am worried about how binding can effect my body. I know that binding can be bad for you, but I am not comfortable when not binding (or wearing something less restrictive, like a sports bra. not comfortable in those, either) and top surgery isn't really plausible right now, and I'm not even really sure about wanting top surgery in the future anyway. so I guess I'm wondering about binding long term and if it's safe or feasible or a good idea.

Binding long term can cause breast tissue damage and binding unsafely long term can complicate getting top surgery. The main worries with binding are rib injuries. However, there haven’t been a lot of studies on the safety of binding (or tucking for that matter) long term or short term. The best you can do is pay attention to your body and if it hurts, stop.

–Ell