Shekswess/llama3_medquad_instruct_dataset huggingface dataset:
Question: what research (or clinical trials) is being done for Motor Neuron Diseases ?
Answer: The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge of the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health (NIH), the leading supporter of biomedical research in the world. Researchers are testing whether different drugs, agents, or interventions are safe and effective in slowing the progression of motor neuron diseasess. NIH is also conducting clinical trials to study drugs to stimulate muscle growth in Kennedys disease and to suppress endogenous retroviruses in individuals with ALS. A large NIH-led collaborative study is investigating the genes and gene activity, proteins, and modifications of adult stem cell models from both healthy people and those with ALS,spinal muscular atrophy, and other neurodegenerative diseases to better understand the function of neurons and other support cells and identify candidate therapeutic compounds.
                

                
conducts research related to the MNDs in its laboratories at the National Institutes of Health (NIH), and also supports additional research through grants to major medical institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as the MNDs.
Question: What is (are) Cerebral Arteriosclerosis ?
Answer: Cerebral arteriosclerosis is the result of thickening and hardening of the walls of the arteries in the brain. Symptoms of cerebral arteriosclerosis include headache, facial pain, and impaired vision.
                
Cerebral arteriosclerosis can cause serious health problems. If the walls of an artery are too thick, or a blood clot becomes caught in the narrow passage, blood flow to the brain can become blocked and cause an ischemic stroke. When the thickening and hardening is uneven, arterial walls can develop bulges (called aneurysms). If a bulge ruptures, bleeding in the brain can cause a hemorrhagic stroke. Both types of stroke can be fatal.
                
Cerebral arteriosclerosis is also related to a condition known as vascular dementia, in which small, symptom-free strokes cause cumulative damage and death to neurons (nerve cells) in the brain. Personality changes in the elderly, such as apathy, weeping, transient befuddlement, or irritability, might indicate that cerebral arteriosclerosis is present in the brain. Computer tomography (CT) and magnetic resonance imaging (MRI) of the brain can help reveal the presence of cerebral arteriosclerosis before ischemic strokes, hemorrhagic strokes, or vascular dementia develop.
Question: What is (are) Pompe Disease ?
Answer: Pompe disease is a rare (estimated at 1 in every 40,000 births), inherited and often fatal disorder that disables the heart and skeletal muscles. It is caused by mutations in a gene that makes an enzyme called acid alpha-glucosidase (GAA). Normally, the body uses GAA to break down glycogen, a stored form of sugar used for energy. The enzyme performs its function in intracellular compartments called lysosomes. Lysosomes are known to function as cellular clearinghouses; they ingest multiple substances including glycogen, which is converted by the GAA into glucose, a sugar that fuels muscles. In Pompe disease, mutations in the GAA gene reduce or completely eliminate this essential enzyme. Excessive amounts of lysosomal glycogen accumulate everywhere in the body, but the cells of the heart and skeletal muscles are the most seriously affected. Researchers have identified up to 300 different mutations in the GAA gene that cause the symptoms of Pompe disease, which can vary widely in terms of age of onset and severity. The severity of the disease and the age of onset are related to the degree of enzyme deficiency.
                
Early onset (or the infantile form) is the result of complete or near complete deficiency of GAA. Symptoms begin in the first months of life, with feeding problems, poor weight gain, muscle weakness, floppiness, and head lag. Respiratory difficulties are often complicated by lung infections. The heart is grossly enlarged. Many infants with Pompe disease also have enlarged tongues. Most babies die from cardiac or respiratory complications before their first birthday.
                
Late onset (or juvenile/adult) Pompe disease is the result of a partial deficiency of GAA. The onset can be as early as the first decade of childhood or as late as the sixth decade of adulthood. The primary symptom is muscle weakness progressing to respiratory weakness and death from respiratory failure after a course lasting several years. The heart is usually not involved. A diagnosis of Pompe disease can be confirmed by screening for the common genetic mutations or measuring the level of GAA enzyme activity in a blood sample. Once Pompe disease is diagnosed, testing of all family members and a consultation with a professional geneticist are recommended. Carriers are most reliably identified via genetic mutation analysis.
Question: What is (are) Alzheimer's Disease ?
Answer: Alzheimer's disease (AD) is an age-related, non-reversible brain disorder that develops over a period of years. Initially, people experience memory loss and confusion, which may be mistaken for the kinds of memory changes that are sometimes associated with normal aging. However, the symptoms of AD gradually lead to behavior and personality changes, a decline in cognitive abilities such as decision-making and language skills, and problems recognizing family and friends. AD ultimately leads to a severe loss of mental function. These losses are related to the worsening breakdown of the connections between certain neurons in the brain and their eventual death. AD is one of a group of disorders called dementias that are characterized by cognitive and behavioral problems. It is the most common cause of dementia among people age 65 and older.
                
There are three major hallmarks in the brain that are associated with the disease processes of AD.
                
- Amyloid plaques, which are made up of fragments of a protein called beta-amyloid peptide mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other nerve cells. - Neurofibrillary tangles (NFTs), found inside neurons, are abnormal collections of a protein called tau. Normal tau is required for healthy neurons. However, in AD, tau clumps together. As a result, neurons fail to function normally and eventually die. - Loss of connections between neurons responsible for memory and learning. Neurons can't survive when they lose their connections to other neurons. As neurons die throughout the brain, the affected regions begin to atrophy, or shrink. By the final stage of AD, damage is widespread and brain tissue has shrunk significantly.
Question: What is the outlook for Alzheimer's Disease ?
Answer: In very few families, people develop AD in their 30s, 40s, and 50s. This is known as "early onset" AD. These individuals have a mutation in one of three different inherited genes that causes the disease to begin at an earlier age. More than 90 percent of AD develops in people older than 65. This form of AD is called "late-onset" AD, and its development and pattern of damage in the brain is similar to that of early-onset AD. The course of this disease varies from person to person, as does the rate of decline. In most people with AD, symptoms first appear after age 65.
                
We don't yet completely understand the causes of late-onset AD, but they probably include genetic, environmental, and lifestyle factors. Although the risk of developing AD increases with age, AD and dementia symptoms are not a part of normal aging. There are also some forms of dementia that aren't related to brain diseases such as AD, but are caused by systemic abnormalities such as metabolic syndrome, in which the combination of high blood pressure, high cholesterol, and diabetes causes confusion and memory loss.
Question: what research (or clinical trials) is being done for Alzheimer's Disease ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS) supports basic and translational research related to AD through grants to major medical institutions across the country. Current studies are investigating how the development of beta amyloid plaques damages neurons, and how abnormalities in tau proteins create the characteristic neurofibrillary tangles of AD. Other research is exploring the impact of risk factors associated with the development of AD, such as pre-existing problems with blood flow in the blood vessels of the brain. Most importantly, the NINDS supports a number of studies that are developing and testing new and novel therapies that can relieve the symptoms of AD and potentially lead to a cure.
                
On May 15, 2012 the Obama Administration announced the release of the National Alzheimers Plan. U.S. Secretary of Health and Human Services Kathleen Sebelius reaffirmed our nations commitment to conquering Alzheimers disease and related dementias, with a specific goal of finding effective ways to prevent and treat the disease by 2025.
Question: What is (are) Meningitis and Encephalitis ?
Answer: Meningitis is an infection of the meninges, the membranes that surround the brain and spinal cord. Encephalitis is inflammation of the brain itself. Causes of encephalitis and meningitis include viruses, bacteria, fungus, and parasites. Anyone can get encephalitis or meningitis.Inflammation from encephalitis and meningitis produce a wide range of symptoms. Symptoms of encephalitis include sudden fever, headache, vomiting, heightened sensitivity to light, stiff neck and back, confusion and impaired judgment, drowsiness, weak muscles, a clumsy and unsteady gait, and irritability. In more severe cases, people may have problems with speech or hearing, vision problems, and hallucinations. Symptoms that might require emergency treatment include loss of consciousness, seizures, muscle weakness, or sudden severe dementia.
                
Symptoms of meningitis, which may appear suddenly, often include high fever, severe and persistent headache, stiff neck, nausea, sensitivity to bright light, and vomiting. Changes in behavior such as confusion, sleepiness, and difficulty waking up may also occur. In infants, symptoms of meningitis or encephalitis may include fever, vomiting, lethargy, body stiffness, unexplained irritability, and a full or bulging fontanel (the soft spot on the top of the head). Anyone experiencing symptoms of meningitis or encephalitis should see a doctor immediately.
Question: What is (are) Deep Brain Stimulation for Parkinson's Disease ?
Answer: Deep brain stimulation (DBS) is a surgical procedure used to treat several disabling neurological symptomsmost commonly the debilitating motor symptoms of Parkinsons disease (PD), such as tremor, rigidity, stiffness, slowed movement, and walking problems. The procedure is also used to treat essential tremor and dystonia. At present, the procedure is used only for individuals whose symptoms cannot be adequately controlled with medications. However, only individuals who improve to some degree after taking medication for Parkinsons benefit from DBS. A variety of conditions may mimic PD but do not respond to medications or DBS. DBS uses a surgically implanted, battery-operated medical device called an implantable pulse generator (IPG) - similar to a heart pacemaker and approximately the size of a stopwatch to - deliver electrical stimulation to specific areas in the brain that control movement, thus blocking the abnormal nerve signals that cause PD symptoms.
                
Before the procedure, a neurosurgeon uses magnetic resonance imaging (MRI) or computed tomography (CT) scanning to identify and locate the exact target within the brain for surgical intervention. Some surgeons may use microelectrode recording - which involves a small wire that monitors the activity of nerve cells in the target area - to more specifically identify the precise brain area that will be stimulated. Generally, these areas are the thalamus, subthalamic nucleus, and globus pallidus. There is a low chance that placement of the stimulator may cause bleeding or infection in the brain.
                
The DBS system consists of three components: the lead, the extension, and the IPG. The lead (also called an electrode)a thin, insulated wireis inserted through a small opening in the skull and implanted in the brain. The tip of the electrode is positioned within the specific brain area. 
                
The extension is an insulated wire that is passed under the skin of the head, neck, and shoulder, connecting the lead to the implantable pulse generator. The IPG (the "battery pack") is the third component and is usually implanted under the skin near the collarbone. In some cases it may be implanted lower in the chest or under the skin over the abdomen.
                
Once the system is in place, electrical impulses are sent from the IPG up along the extension wire and the lead and into the brain. These impulses block abnormal electrical signals and alleviate PD motor symptoms.
Question: what research (or clinical trials) is being done for Deep Brain Stimulation for Parkinson's Disease ?
Answer: The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National institutes of Health (NIH), supports research on DBS to determine its safety, reliability, and effectiveness as a treatment for PD. NINDS supported research on brain circuitry was critical to the development of DBS.
                
Researchers are continuing to study DBS and to develop ways of improving it. A two-part study funded by the NINDS and the Department of Veterans Affairs first compared bilateral DBS to best medical therapy, including medication adjustment and physical therapy. Bilateral DBS showed overall superiority to best medical therapy at improving motor symptoms and quality of life. The second part of the study, involving nearly 300 patients, compared subthalamic nucleus (STN) DBS to globus pallidus interna (GPI) DBS. The two groups reported similar improvements in motor control and quality of life in scores on the Unified Parkinsons Disease Rating Scale. On a variety of neuropsychological tests, there were no significant differences between the two groups. However, the STN DBS group experienced a greater decline on a test of visuomotor processing speed, which measures how quickly someone thinks and acts on information. Also, the STN DBS group had slight worsening on a standard assessment of depression, while the GPI DBS group had slight improvement on the same test. The importance of these two differences is not clear, and will be scrutinized in follow-up research.
                
In addition, NINDS-supported researchers are developing and testing improved implantable pulse generators, and conducting studies to better understand the therapeutic effect of neurostimulation on neural circuitry and brain regions affected in PD. For more information about current studies on brain stimulation and Parkinsons disease, see www.clinicaltrials.gov and search for deep brain stimulation AND Parkinson AND NINDS. For information about NINDS-and NIH-supported research studies in this area, see the NIH RePORTER (Research Portfolio Online Reporting Tools) at http://projectreporter.nih.gov and search for deep brain stimulation AND Parkinson.
                
The Brain Initiative for Advancing Innovative Neurotechnologies (BRAIN) initiative, announced in 2013, offers unprecedented opportunities to unlock the mysteries of the brain and accelerate the development of research and technologies to treat disorders such as Parkinsons disease. For more information about the BRAIN initiative, see www.nih.gov/science/brain.
Question: What is (are) Mineral and Bone Disorder in Chronic Kidney Disease ?
Answer: Mineral and bone disorder in CKD occurs when damaged kidneys and abnormal hormone levels cause calcium and phosphorus levels in a persons blood to be out of balance. Mineral and bone disorder commonly occurs in people with CKD and affects most people with kidney failure receiving dialysis.
                
In the past, health care providers used the term renal osteodystrophy to describe mineral and hormone disturbances caused by kidney disease. Today, renal osteodystrophy only describes bone problems that result from mineral and bone disorder in CKD. Health care providers might use the phrase chronic kidney disease mineral and bone disorder, or CKD-MBD, to describe the condition that affects the bones, heart, and blood vessels.
Question: What causes Mineral and Bone Disorder in Chronic Kidney Disease ?
Answer: Chronic kidney disease causes mineral and bone disorder because the kidneys do not properly balance the mineral levels in the body. The kidneys
                
- stop activating calcitriol. The low levels of calcitriol in the body create an imbalance of calcium in the blood.  - do not remove the phosphorus in the blood properly, so phosphorus levels rise in the blood. The extra phosphorus pulls calcium out of the bones, causing them to weaken.
                
Another factor contributes to the cause of mineral and bone disorder. When the kidneys are damaged, the parathyroid gland releases parathyroid hormone into the blood to pull calcium from the bones and raise blood calcium levels. This response restores the balance of phosphorus and calcium; however, it also starves the bones of much-needed calcium.
Question: What are the symptoms of Mineral and Bone Disorder in Chronic Kidney Disease ?
Answer: In adults, symptoms of mineral and bone disorder in CKD may not appear until bone changes have taken place for many years. For this reason, people often refer to the disease as a silent crippler. Eventually, a person with the condition may begin to feel bone and joint pain.
                

                
Mineral and Bone Disorder in Children with Chronic Kidney Disease   Mineral and bone disorder in CKD is most serious when it occurs in children because their bones are still developing and growing. Growing children can show symptoms of mineral and bone disorder even in the early stages of CKD. Slowed bone growth leads to short stature, which may remain with a child into adulthood. One deformity caused by mineral and bone disorder in CKD occurs when the legs bend inward or outward, a condition often referred to as "renal rickets." More information is provided in the NIDDK health topic, Growth Failure in Children with Kidney Disease. Find more about childrens bone health on the Eunice Kennedy Shriver National Institute of Child Health and Human Development website at www.nichd.nih.gov.
Question: What are the complications of Mineral and Bone Disorder in Chronic Kidney Disease ?
Answer: The complications of mineral and bone disorder in CKD include slowed bone growth and deformities, and heart and blood vessel problems.
                
Slowed Bone Growth and Deformities
                
Damaged kidneys must work harder to clear phosphorus from the body. High levels of phosphorus cause lower levels of calcium in the blood, resulting in the following series of events:
                
- When a persons blood calcium level becomes too low, the parathyroid glands release parathyroid hormone.  - Parathyroid hormone removes calcium from bones and places it into the blood, raising a persons blood calcium level at the risk of harming bones.  - A low calcitriol level also leads to an increased level of parathyroid hormone.
                
If mineral and bone disorder in CKD remains untreated in adults, bones gradually become thin and weak, and a person with the condition may begin to feel bone and joint pain. Mineral and bone disorder in CKD also increases a persons risk of bone fractures.
                
Heart and Blood Vessel Problems
                
In addition to harming bones, mineral and bone disorder in CKD can cause problems in the heart and blood vessels:
                
- High levels of blood calcium can damage blood vessels and lead to heart problems.  - High phosphorus levels also can cause blood vessels to become like bone, leading to hardening of the arteries.  - High phosphorus levels also cause abnormal hormone regulation, even if the calcium level is acceptable.
                
Parathyroid hormone and another hormone made in the bones called FGF23 can also affect bone and heart health, leading to the following series of problems:
                
- When parathyroid hormone or FGF23 levels are high, a person can have heart problems.   - The complex hormone abnormalities that cause bone deformities can also harm a persons heart and blood vessels.
Question: How to diagnose Mineral and Bone Disorder in Chronic Kidney Disease ?
Answer: A health care provider diagnoses mineral and bone disorder in CKD with
                
- a family and medical history  - a physical exam  - a blood test  - a bone biopsy  - an x-ray
                
Family and Medical History
                
Taking a medical and family history is one of the first things a health care provider may do to help diagnose mineral and bone disorder in CKD. He or she will ask the patient or caretaker questions about when the patient was first diagnosed with CKD and whether any family members have also had mineral and bone disorder with or without CKD.
                
Physical Exam
                
A physical exam may help diagnose mineral and bone disorder in CKD. During a physical exam, a health care provider usually examines a patients body for changes in bone structure.
                
Blood Test
                
A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The blood test shows levels of calcium, phosphorus, parathyroid hormone, and sometimes vitamin D.
                
Bone Biopsy
                
A bone biopsy is a procedure that removes a piece of bone tissue for examination with a microscope. A health care provider performs the biopsy in a hospital with light sedation and local anesthetic. The health care provider uses imaging techniques such as ultrasound or a computerized tomography scan to guide the biopsy needle into the hip bone. A pathologista doctor who specializes in diagnosing diseasesexamines the bone tissue in a lab. The test can show whether a persons bone cells are building normal bone.
                
X-ray
                
An x-ray is a picture created by using radiation and recorded on film or on a computer. The amount of radiation used is small. A radiographer performs the x-ray at a hospital or an outpatient center, and a radiologista doctor who specializes in medical imaginginterprets the images. Patients do not need anesthesia. The patient will lie on a table or stand during the x-ray. The technician will position the x-ray machine over the bone area. The patient will hold his or her breath as the x-ray machine takes the picture so that the picture will not be blurry. The radiographer may ask the patient to change position for additional pictures. An x-ray can show extra calcium in blood vessels.
                
Each of these tests can help the health care provider determine whether CKD or some other condition is causing the mineral and bone disorder and decide on a course of treatment.