A precursor of noradrenaline that is used in the treatment of parkinsonism. The racemic form (DL-threo-3,4-dihydroxyphenylserine) has also been used, and has been investigated in the treatment of orthostatic hypotension. There is a deficit of noradrenaline as well as of dopamine in Parkinson's disease and it has been proposed that this underlies the sudden transient freezing seen usually in advanced disease. Administration of DL-threo-3,4-dihydroxyphenylserine has been claimed to result in an improvement in this phenomenon but controlled studies have failed to demonstrate improvement. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)
The presence of organisms, or any foreign material that makes a drug preparation impure.
A deaminated metabolite of LEVODOPA.
A significant drop in BLOOD PRESSURE after assuming a standing position. Orthostatic hypotension is a finding, and defined as a 20-mm Hg decrease in systolic pressure or a 10-mm Hg decrease in diastolic pressure 3 minutes after the person has risen from supine to standing. Symptoms generally include DIZZINESS, blurred vision, and SYNCOPE.
Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists.
Inherited disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. The different clinical types based on symptoms correspond to the presence of a variety of mutations in several different proteins including transthyretin (PREALBUMIN); APOLIPOPROTEIN A-I; and GELSOLIN.
Disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. Familial, primary (nonfamilial), and secondary forms have been described. Some familial subtypes demonstrate an autosomal dominant pattern of inheritance. Clinical manifestations include sensory loss, mild weakness, autonomic dysfunction, and CARPAL TUNNEL SYNDROME. (Adams et al., Principles of Neurology, 6th ed, p1349)
A syndrome complex composed of three conditions which represent clinical variants of the same disease process: STRIATONIGRAL DEGENERATION; SHY-DRAGER SYNDROME; and the sporadic form of OLIVOPONTOCEREBELLAR ATROPHIES. Clinical features include autonomic, cerebellar, and basal ganglia dysfunction. Pathologic examination reveals atrophy of the basal ganglia, cerebellum, pons, and medulla, with prominent loss of autonomic neurons in the brain stem and spinal cord. (From Adams et al., Principles of Neurology, 6th ed, p1076; Baillieres Clin Neurol 1997 Apr;6(1):187-204; Med Clin North Am 1999 Mar;83(2):381-92)
Diseases of the parasympathetic or sympathetic divisions of the AUTONOMIC NERVOUS SYSTEM; which has components located in the CENTRAL NERVOUS SYSTEM and PERIPHERAL NERVOUS SYSTEM. Autonomic dysfunction may be associated with HYPOTHALAMIC DISEASES; BRAIN STEM disorders; SPINAL CORD DISEASES; and PERIPHERAL NERVOUS SYSTEM DISEASES. Manifestations include impairments of vegetative functions including the maintenance of BLOOD PRESSURE; HEART RATE; pupil function; SWEATING; REPRODUCTIVE AND URINARY PHYSIOLOGY; and DIGESTION.
A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease.
NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.
It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)
Patient health knowledge related to medications including what is being used and why as well as instructions and precautions.
Services providing pharmaceutic and therapeutic drug information and consultation.
Societies whose membership is limited to pharmacists.
Advanced programs of training to meet certain professional requirements in fields other than medicine or dentistry, e.g., pharmacology, nutrition, nursing, etc.
I'm sorry for any confusion, but the term "Maryland" is not a recognized medical term with a specific definition in the medical field. It refers to a state in the United States. If you have any questions about a medical condition or treatment, I would be happy to try and help answer those!

L-DOPS-Accelerated recovery of locomotor function in rats subjected to sensorimotor cortex ablation injury: pharmacobehavioral studies. (1/30)

Central norepinephrine (NE) has been shown to play a beneficial role in amphetamine-facilitated recovery of behavior. To give insight into understanding the mechanism, the present studies were conducted to examine (a) the effects of L-threo-3,4-dihydroxyphenylserine (L-DOPS) combined with benserazide (BSZ; a peripheral aromatic amino acid decarboxylase inhibitor) and L-3,4-dihydroxyphenylalanine (L-DOPA), precursors of NE and dopamine (DA), respectively, on the recovery from beam-walking performance deficits in rats subjected to unilateral sensorimotor cortex ablation injury, and (b) the relationships between the behavioral recovery and the frequency of postoperative training and the size of ablation injury. It was found that the combined treatments with L-DOPS and BSZ promoted the recovery of locomotor function as early as 24 hours after injury. L-DOPA alone, however, did not facilitate behavioral recovery. The results of assay for the tissue levels of NE and its major metabolite (3-methoxy-4-hydoxyphenylethylene glycol; MHPG) in the brain using high-pressure liquid chromotography showed MHPG, but not NE, significantly increased in the cerebellum and the hippocampus. The behavioral recovery was also significantly correlated with the frequency of training subsequent to injury, but inversely with the size of cortex ablation. These results suggest that NE is likely to modulate functional recovery in this rodent model.  (+info)

Norepinephrine precursor therapy in neurogenic orthostatic hypotension. (2/30)

BACKGROUND: In patients with neurogenic orthostatic hypotension (NOH), the availability of the sympathetic neurotransmitter norepinephrine (NE) in the synaptic cleft is insufficient to maintain blood pressure while in the standing posture. METHODS AND RESULTS: We determined the effect of oral administration of the synthetic amino acid L-threo-3,4-dihydroxyphenylserine (L-DOPS), which is decarboxylated to NE by the enzyme L-aromatic amino acid decarboxylase (L-AADC) in neural and nonneural tissue, on blood pressure and orthostatic tolerance in 19 patients with severe NOH (8 with pure autonomic failure and 11 with multiple-system atrophy). A single-blind dose-titration study determined the most appropriate dose for each patient. Patients were then enrolled in a double-blind, placebo-controlled, crossover trial. L-DOPS significantly raised mean blood pressure both supine (from 101+/-4 to 141+/-5 mm Hg) and standing (from 60+/-4 to 100+/-6 mm Hg) for several hours and improved orthostatic tolerance in all patients. After L-DOPS, blood pressure increases were closely associated with increases in plasma NE levels. Oral administration of carbidopa, which inhibits L-AADC outside the blood-brain barrier, blunted both the increase in plasma NE and the pressor response to L-DOPS in all patients CONCLUSIONS: Acute administration of L-DOPS increases blood pressure and improves orthostatic tolerance in patients with NOH. The pressor effect results from conversion of L-DOPS to NE outside the central nervous system.  (+info)

Norepinephrine-deficient mice lack responses to antidepressant drugs, including selective serotonin reuptake inhibitors. (3/30)

Mice unable to synthesize norepinephrine (NE) and epinephrine due to targeted disruption of the dopamine beta-hydroxylase gene, Dbh, were used to critically test roles for NE in mediating acute behavioral changes elicited by different classes of antidepressants. To this end, we used the tail suspension test, one of the most widely used paradigms for assessing antidepressant activity and depression-related behaviors in normal and genetically modified mice. Dbh(-/-) mice failed to respond to the behavioral effects of various antidepressants, including the NE reuptake inhibitors desipramine and reboxetine, the monoamine oxidase inhibitor pargyline, and the atypical antidepressant bupropion, even though they did not differ in baseline immobility from Dbh(+/-) mice, which have normal levels of NE. Surprisingly, the effects of the selective serotonin reuptake inhibitors (SSRIs) fluoxetine, sertraline, and paroxetine were also absent or severely attenuated in the Dbh(-/-) mice. In contrast, citalopram (the most selective SSRI) was equally effective at reducing immobility in mice with and without NE. Restoration of NE by using L-threo-3,4-dihydroxyphenylserine reinstated the behavioral effects of both desipramine and paroxetine in Dbh(-/-) mice, thus demonstrating that the reduced sensitivity to antidepressants is related to NE function, as opposed to developmental abnormalities resulting from chronic NE deficiency. Microdialysis studies demonstrated that the ability of fluoxetine to increase hippocampal serotonin was blocked in Dbh(-/-) mice, whereas citalopram's effect was only partially attenuated. These data show that NE plays an important role in mediating acute behavioral and neurochemical actions of many antidepressants, including most SSRIs.  (+info)

A requirement for memory retrieval during and after long-term extinction learning. (4/30)

Current learning theories are based on the idea that learning is driven by the difference between expectations and experience (the delta rule). In extinction, one learns that certain expectations no longer apply. Here, we test the potential validity of the delta rule by manipulating memory retrieval (and thus expectations) during extinction learning. Adrenergic signaling is critical for the time-limited retrieval (but not acquisition or consolidation) of contextual fear. Using genetic and pharmacologic approaches to manipulate adrenergic signaling, we find that long-term extinction requires memory retrieval but not conditioned responding. Identical manipulations of the adrenergic system that do not affect memory retrieval do not alter extinction. The results provide substantial support for the delta rule of learning theory. In addition, the timing over which extinction is sensitive to adrenergic manipulation suggests a model whereby memory retrieval occurs during, and several hours after, extinction learning to consolidate long-term extinction memory.  (+info)

L-threo 3,4-dihydroxyphenylserine treatment during mouse perinatal and rat postnatal development does not alter the impact of dietary copper deficiency. (5/30)

Dietary copper (Cu) deficiency was induced perinatally in Swiss Albino mice and postnatally in male Holtzman rats to investigate the effect of L-threo 3,4-dihydroxyphenylserine (DOPS) on pup survival and catecholamine levels in a 2 x 2 factorial design. Mouse dams were placed on one of four treatments 14 days after mating and rats at postnatal day 19 (P19). Treatments were Cu-adequate (Cu + ) and Cu-deficient (Cu - ) diets with or without DOPS (1 mg/ml) in the drinking water. Mouse pups were killed at P14 and rats at P49. Mortality in Cu - pups was 46% and not significantly improved by DOPS, 39%. A repeat study with mice adding ascorbic acid in the water with DOPS showed no improvement. Compared to Cu + animals, Cu - animals were smaller, anemic and had a 92% reduction in liver Cu. DOPS treatment made no improvement to and in some cases exacerbated the Cu deficiency. Catecholamine levels measured in heart and brain by LCEC showed decreased NE levels and increased DA levels in Cu - animals compared to controls. DOPS treatment did not alter this pattern. Although DOPS was present in treated animal's tissues, survival in mice and catecholamine levels in mice and rats were not altered by the 1 mg/ml dose of DOPS.  (+info)

Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate reward. (6/30)

Norepinephrine (NE) is widely implicated in opiate withdrawal, but much less is known about its role in opiate-induced locomotion and reward. In mice lacking dopamine beta-hydroxylase (DBH), an enzyme critical for NE synthesis, we found that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomotion. These deficits were rescued by systemic NE restoration. Viral restoration of DBH expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for morphine. Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward.  (+info)

The actions of dihydroxyphenylalanine and dihydroxyphenylserine on the sleep-wakefulness cycle of the rat after peripheral decarboxylase inhibition. (7/30)

1. The actions of dihydroxyphenylalanine (DOPA) and dihydroxyphenylserine (DOPS) were assessed on the sleep-wakefulness cycle of male Wistar rats. 2. In comparative studies the extracerebral decarboxylase was inhibited with serinetrihydroxybenzylhydrazide (RO 4-4602) before injection of DOPA or DOPS. 3. DOPA (80-160 mg/kg, i.p.) with or without previous inhibition of the peripheral decarboxylase gave rise to an initial significant increase of slow wave activity, which may be related to a release of 5-hydroxytryptamine. 4. During the subsequent 8 h sessions, DOPA significantly decreased slow wave sleep and rapid eye movement sleep (REM) and increased wakefulness. 5. DOPS (80-160 mg/kg, i.p.) did not significantly modify the sleep-wakefulness cycle apart from a decrease of the latency for the first REM episode after 160 mg/kg in the RO 4-4602 pretreated animals.  (+info)

Dopamine beta-hydroxylase deficiency. A genetic disorder of cardiovascular regulation. (8/30)

Dopamine beta-hydroxylase (DBH) deficiency is a genetic disorder in which affected patients cannot synthesize norepinephrine, epinephrine, and octopamine in either the central nervous system or the peripheral autonomic neurons. Dopamine acts as a false neurotransmitter in their noradrenergic neurons. Neonates with DBH deficiency have had episodic hypothermia, hypoglycemia, and hypotension, but survivors sometimes cope relatively well until late childhood when overwhelming orthostatic hypotension profoundly limits their activities. The hypotension may be so severe that clonic seizures supervene. Most currently recognized patients are young or middle-aged adults. The diagnosis is established by the observation of severe orthostatic hypotension in a patient whose plasma norepinephrine/dopamine ratio is much less than one.  (+info)

Droxidopa is a medication that is used to treat neurogenic orthostatic hypotension, which is a condition characterized by a drop in blood pressure when standing up from a seated or lying down position. Droxidopa works by helping the body to maintain normal levels of norepinephrine, a hormone and neurotransmitter that helps to regulate blood pressure.

Droxidopa is a synthetic precursor of norepinephrine, which means that it is converted into norepinephrine in the body. By increasing the availability of norepinephrine, droxidopa helps to constrict blood vessels and increase blood pressure, reducing symptoms of orthostatic hypotension such as dizziness, lightheadedness, and fainting.

Droxidopa is available in capsule form and is typically taken three times a day with food. It may take several weeks of treatment before the full benefits of droxidopa are seen. Common side effects of droxidopa include headache, dizziness, and fatigue.

Drug contamination refers to the presence of impurities or foreign substances in a pharmaceutical drug or medication. These impurities can include things like bacteria, chemicals, or other drugs that are not intended to be present in the final product. Drug contamination can occur at any stage during the production, storage, or distribution of a medication and can potentially lead to reduced effectiveness, increased side effects, or serious health risks for patients. It is closely monitored and regulated by various health authorities to ensure the safety and efficacy of medications.

3,4-Dihydroxyphenylacetic Acid (3,4-DOPAC) is a major metabolite of dopamine, which is a neurotransmitter in the brain. Dopamine is metabolized by the enzyme monoamine oxidase to form dihydroxyphenylacetaldehyde, which is then further metabolized to 3,4-DOPAC by the enzyme aldehyde dehydrogenase.

3,4-DOPAC is found in the urine and can be used as a marker for dopamine turnover in the brain. Changes in the levels of 3,4-DOPAC have been associated with various neurological disorders such as Parkinson's disease and schizophrenia. Additionally, 3,4-DOPAC has been shown to have antioxidant properties and may play a role in protecting against oxidative stress in the brain.

Orthostatic hypotension is a type of low blood pressure that occurs when you stand up from a sitting or lying position. The drop in blood pressure causes a brief period of lightheadedness or dizziness, and can even cause fainting in some cases. This condition is also known as postural hypotension.

Orthostatic hypotension is caused by a rapid decrease in blood pressure when you stand up, which reduces the amount of blood that reaches your brain. Normally, when you stand up, your body compensates for this by increasing your heart rate and constricting blood vessels to maintain blood pressure. However, if these mechanisms fail or are impaired, orthostatic hypotension can occur.

Orthostatic hypotension is more common in older adults, but it can also affect younger people who have certain medical conditions or take certain medications. Some of the risk factors for orthostatic hypotension include dehydration, prolonged bed rest, pregnancy, diabetes, heart disease, Parkinson's disease, and certain neurological disorders.

If you experience symptoms of orthostatic hypotension, it is important to seek medical attention. Your healthcare provider can perform tests to determine the underlying cause of your symptoms and recommend appropriate treatment options. Treatment may include lifestyle changes, such as increasing fluid intake, avoiding alcohol and caffeine, and gradually changing positions from lying down or sitting to standing up. In some cases, medication may be necessary to manage orthostatic hypotension.

Antiparkinson agents are a class of medications used to treat the symptoms of Parkinson's disease and related disorders. These agents work by increasing the levels or activity of dopamine, a neurotransmitter in the brain that is responsible for regulating movement and coordination.

There are several types of antiparkinson agents, including:

1. Levodopa: This is the most effective treatment for Parkinson's disease. It is converted to dopamine in the brain and helps to replace the missing dopamine in people with Parkinson's.
2. Dopamine agonists: These medications mimic the effects of dopamine in the brain and can be used alone or in combination with levodopa. Examples include pramipexole, ropinirole, and rotigotine.
3. Monoamine oxidase B (MAO-B) inhibitors: These medications block the breakdown of dopamine in the brain and can help to increase its levels. Examples include selegiline and rasagiline.
4. Catechol-O-methyltransferase (COMT) inhibitors: These medications block the breakdown of levodopa in the body, allowing it to reach the brain in higher concentrations. Examples include entacapone and tolcapone.
5. Anticholinergic agents: These medications block the action of acetylcholine, another neurotransmitter that can contribute to tremors and muscle stiffness in Parkinson's disease. Examples include trihexyphenidyl and benztropine.

It is important to note that antiparkinson agents can have side effects, and their use should be carefully monitored by a healthcare professional. The choice of medication will depend on the individual patient's symptoms, age, overall health, and other factors.

Familial amyloid neuropathies are a group of inherited disorders characterized by the accumulation of abnormal deposits of amyloid proteins in various tissues and organs of the body. These abnormal deposits can cause damage to nerves, leading to a peripheral neuropathy that affects sensation, movement, and organ function.

There are several types of familial amyloid neuropathies, each caused by different genetic mutations. The most common type is known as transthyretin-related hereditary amyloidosis (TTR-HA), which is caused by mutations in the TTR gene. Other types include apolipoprotein A1-related hereditary amyloidosis (APOA1-HA) and gelsolin-related amyloidosis (AGel-HA).

Symptoms of familial amyloid neuropathies can vary depending on the type and severity of the disorder. Common symptoms include:

* Numbness, tingling, or pain in the hands and feet
* Weakness or loss of muscle strength in the legs and arms
* Autonomic nervous system dysfunction, leading to problems with digestion, heart rate, blood pressure, and temperature regulation
* Carpal tunnel syndrome
* Eye abnormalities, such as vitreous opacities or retinal deposits
* Kidney disease

Familial amyloid neuropathies are typically inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutated gene from an affected parent. Diagnosis is usually made through genetic testing and confirmation of the presence of amyloid deposits in tissue samples.

Treatment for familial amyloid neuropathies typically involves managing symptoms and slowing the progression of the disease. This may include medications to control pain, physical therapy to maintain muscle strength and mobility, and devices such as braces or wheelchairs to assist with mobility. In some cases, liver transplantation may be recommended to remove the source of the mutated transthyretin protein.

Amyloid neuropathies are a group of peripheral nerve disorders caused by the abnormal accumulation of amyloid proteins in the nerves. Amyloid is a protein that can be produced in various diseases and can deposit in different organs, including nerves. When this occurs in the nerves, it can lead to damage and dysfunction, resulting in symptoms such as numbness, tingling, pain, and weakness in the affected limbs.

There are several types of amyloid neuropathies, with the two most common being:

1. Transthyretin (TTR)-related hereditary amyloidosis: This is an inherited disorder caused by mutations in the TTR gene, which leads to the production of abnormal TTR protein that can form amyloid deposits in various organs, including nerves.
2. Immunoglobulin light chain (AL) amyloidosis: This is a disorder in which abnormal plasma cells produce excessive amounts of immunoglobulin light chains, which can form amyloid deposits in various organs, including nerves.

The diagnosis of amyloid neuropathies typically involves a combination of clinical evaluation, nerve conduction studies, and tissue biopsy to confirm the presence of amyloid deposits. Treatment options depend on the underlying cause of the disorder and may include medications, chemotherapy, stem cell transplantation, or supportive care to manage symptoms.

Multiple System Atrophy (MSA) is a rare, progressive neurodegenerative disorder that affects multiple systems in the body. It is characterized by a combination of symptoms including Parkinsonism (such as stiffness, slowness of movement, and tremors), cerebellar ataxia (lack of muscle coordination), autonomic dysfunction (problems with the autonomic nervous system which controls involuntary actions like heart rate, blood pressure, sweating, and digestion), and pyramidal signs (abnormalities in the corticospinal tracts that control voluntary movements).

The disorder is caused by the degeneration of nerve cells in various parts of the brain and spinal cord, leading to a loss of function in these areas. The exact cause of MSA is unknown, but it is thought to involve a combination of genetic and environmental factors. There is currently no cure for MSA, and treatment is focused on managing symptoms and improving quality of life.

The Autonomic Nervous System (ANS) is a part of the nervous system that controls involuntary actions, such as heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. It consists of two subdivisions: the sympathetic and parasympathetic nervous systems, which generally have opposing effects and maintain homeostasis in the body.

Autonomic Nervous System Diseases (also known as Autonomic Disorders or Autonomic Neuropathies) refer to a group of conditions that affect the functioning of the autonomic nervous system. These diseases can cause damage to the nerves that control automatic functions, leading to various symptoms and complications.

Autonomic Nervous System Diseases can be classified into two main categories:

1. Primary Autonomic Nervous System Disorders: These are conditions that primarily affect the autonomic nervous system without any underlying cause. Examples include:
* Pure Autonomic Failure (PAF): A rare disorder characterized by progressive loss of autonomic nerve function, leading to symptoms such as orthostatic hypotension, urinary retention, and constipation.
* Multiple System Atrophy (MSA): A degenerative neurological disorder that affects both the autonomic nervous system and movement coordination. Symptoms may include orthostatic hypotension, urinary incontinence, sexual dysfunction, and Parkinsonian features like stiffness and slowness of movements.
* Autonomic Neuropathy associated with Parkinson's Disease: Some individuals with Parkinson's disease develop autonomic symptoms such as orthostatic hypotension, constipation, and urinary dysfunction due to the degeneration of autonomic nerves.
2. Secondary Autonomic Nervous System Disorders: These are conditions that affect the autonomic nervous system as a result of an underlying cause or disease. Examples include:
* Diabetic Autonomic Neuropathy: A complication of diabetes mellitus that affects the autonomic nerves, leading to symptoms such as orthostatic hypotension, gastroparesis (delayed gastric emptying), and sexual dysfunction.
* Autoimmune-mediated Autonomic Neuropathies: Conditions like Guillain-Barré syndrome or autoimmune autonomic ganglionopathy can cause autonomic symptoms due to the immune system attacking the autonomic nerves.
* Infectious Autonomic Neuropathies: Certain infections, such as HIV or Lyme disease, can lead to autonomic dysfunction as a result of nerve damage.
* Toxin-induced Autonomic Neuropathy: Exposure to certain toxins, like heavy metals or organophosphate pesticides, can cause autonomic neuropathy.

Autonomic nervous system disorders can significantly impact a person's quality of life and daily functioning. Proper diagnosis and management are crucial for improving symptoms and preventing complications. Treatment options may include lifestyle modifications, medications, and in some cases, devices or surgical interventions.

Prealbumin, also known as transthyretin, is a protein produced primarily in the liver and circulates in the blood. It plays a role in transporting thyroid hormones and vitamin A throughout the body. Prealbumin levels are often used as an indicator of nutritional status and liver function. Low prealbumin levels may suggest malnutrition or inflammation, while increased levels can be seen in certain conditions like hyperthyroidism. It is important to note that prealbumin levels should be interpreted in conjunction with other clinical findings and laboratory tests for a more accurate assessment of a patient's health status.

MedlinePlus is not a medical term, but rather a consumer health website that provides high-quality, accurate, and reliable health information, written in easy-to-understand language. It is produced by the U.S. National Library of Medicine, the world's largest medical library, and is widely recognized as a trusted source of health information.

MedlinePlus offers information on various health topics, including conditions, diseases, tests, treatments, and wellness. It also provides access to drug information, medical dictionary, and encyclopedia, as well as links to clinical trials, medical news, and patient organizations. The website is available in both English and Spanish and can be accessed for free.

Copyright is a legal concept that gives the creator of an original work exclusive rights to its use and distribution, usually for a limited period of time. In the medical field, copyright protection can apply to various works such as medical textbooks, journal articles, educational materials, software, and multimedia presentations. It is important to note that copyright law seeks to strike a balance between protecting the rights of creators and promoting the progress of science and knowledge by allowing for limited use of copyrighted material under certain circumstances, such as fair use.

It's worth mentioning that while copyright protection can apply to medical works, there are also exceptions and limitations to copyright law that may allow for the use of copyrighted material without permission from the copyright owner in certain situations. For example, in the United States, the "fair use" doctrine allows for limited use of copyrighted material without obtaining permission from the copyright owner, depending on factors such as the purpose and character of the use, the nature of the copyrighted work, the amount and substantiality of the portion used, and the effect of the use upon the potential market for or value of the copyrighted work.

When using medical works that are protected by copyright, it is important to obtain permission from the copyright owner or ensure that the use falls under an exception or limitation to copyright law, such as fair use, in order to avoid infringing on the exclusive rights of the copyright owner.

Patient medication knowledge, also known as patient medication literacy or medication adherence, refers to the ability of a patient to understand and effectively communicate about their medications, including what they are for, how and when to take them, potential side effects, and other important information. This is an essential component of medication management, as it allows patients to properly follow their treatment plans and achieve better health outcomes. Factors that can affect patient medication knowledge include age, education level, language barriers, and cognitive impairments. Healthcare providers play a key role in promoting patient medication knowledge by providing clear and concise instructions, using visual aids when necessary, and regularly assessing patients' understanding of their medications.

Drug Information Services (DIS) are specialized resources within healthcare systems, typically staffed by clinical pharmacists and pharmacy residents, that provide evidence-based information and analysis about medications to healthcare professionals and patients. The primary goal of DIS is to optimize medication use and improve patient outcomes through the provision of accurate, unbiased, and timely information on drug therapy.

DIS commonly provide a range of services, including:

1. Answering medication-related questions from healthcare providers, such as physicians, nurses, and other pharmacists, regarding drug interactions, dosing, adverse effects, and therapeutic alternatives.
2. Developing and maintaining formulary management systems to ensure the safe and cost-effective use of medications within a healthcare institution or system.
3. Providing patient education materials and resources on medication therapy, including proper administration techniques, potential side effects, and storage requirements.
4. Conducting ongoing literature evaluations and synthesizing evidence-based recommendations for medication use in various clinical scenarios.
5. Collaborating with healthcare teams to develop and implement guidelines, policies, and procedures related to medication management and safety.
6. Offering educational programs and resources for healthcare professionals and students to enhance their knowledge of pharmacotherapy and medication safety practices.
7. Participating in multidisciplinary committees focused on improving medication use processes, reducing medication errors, and promoting patient safety.

DIS are essential components of modern healthcare systems, as they help ensure the safe, effective, and efficient use of medications for improved patient outcomes.

A pharmaceutical society is a professional organization that represents and serves the interests of pharmacists and the pharmaceutical industry in a given society or country. The primary objective of these societies is to promote the advancement of the profession of pharmacy, including education, research, and practice. They also work to ensure the safe and effective use of medications, advocate for evidence-based policies and practices, and provide resources and support to their members.

Pharmaceutical societies may engage in various activities, such as:

1. Developing guidelines and standards for pharmacy education and practice.
2. Providing continuing education programs for pharmacists.
3. Conducting research and disseminating knowledge related to pharmacy and medication use.
4. Advocating for policies that promote the safe and effective use of medications.
5. Collaborating with other healthcare professionals, regulatory bodies, and industry partners to improve patient outcomes.
6. Providing resources and support to members, including career development opportunities and networking events.

Examples of pharmaceutical societies include the American Pharmacists Association (APhA), the Royal Pharmaceutical Society (RPS) in the UK, and the International Pharmaceutical Federation (FIP).

A non-medical internship is not specifically related to the field of medicine. It generally refers to an organized period of work experience, often temporary, in which a person typically a student or trainee, gains practical knowledge and skills in a particular industry or profession. The intern is supervised and mentored by experienced professionals in the field. Non-medical internships can be found in various sectors such as business, engineering, law, education, media, technology, and many others. They provide an opportunity to apply theoretical knowledge gained in the classroom to real-world situations and help interns develop professional competencies and networks.

I'm sorry for any confusion, but "Maryland" is a proper noun and does not have a medical definition. It is a state located in the Mid-Atlantic region of the United States. However, if you are referring to a specific medical term or concept that includes "Maryland," could you please provide more context? I'll do my best to help with accurate information based on the provided context.

... droxidopa is a precursor and prodrug of norepinephrine.[citation needed] Droxidopa was developed by Sumitomo Pharmaceuticals ... Droxidopa (INN; trade name Northera; also known as L-DOPS, L-threo-dihydroxyphenylserine, L-threo-DOPS and SM-5688) is a ... Droxidopa can also cross the blood-brain barrier (BBB) where it is converted to norepinephrine from within the brain. Increased ... Droxidopa is a prodrug of norepinephrine used to increase the concentrations of these neurotransmitters in the body and brain. ...
Droxidopa treatment, and the effect on orthostatic tolerance and glucose homeostasis. It was found that Droxidopa increased ... However, the use of Droxidopa was found to only produce "modest changes in glucose homeostasis" overall. This shows that ... Since the conversion of dihydroxyphenylserine (Droxidopa; trade name: Northera; also known as L-DOPS, L-threo- ... droxidopa) in the management of neurogenic orthostatic hypotension: a multi-national, multi-center, dose-ranging study in ...
ISBN 978-0-19-182714-3. Ruzieh M, Dasa O, Pacenta A, Karabin B, Grubb B (2017). "Droxidopa in the Treatment of Postural ...
... droxidopa) Dopamine (Intropan, Inovan, Revivan, Rivimine, Dopastat, Dynatra, etc.) Norepinephrine (noradrenaline; Levophed, etc ...
Drugs such as midodrine, fludrocortisone, droxidopa, and pyridostigmine are sometimes prescribed to help stabilize blood ...
Droxidopa) Methyldopa (Aldomet, Apo-Methyldopa, Dopamet, Novomedopa, etc.) Dopamine (Intropan, Inovan, Revivan, Rivimine, ...
l-DOPA (Levodopa; Sinemet, Parcopa, Atamet, Stalevo, Madopar, Prolopa, etc.) l-DOPS (Droxidopa) Methyldopa (Aldomet, Apo- ...
"Standing and Supine Blood Pressure Outcomes Associated with Droxidopa and Midodrine in Patients with Neurogenic Orthostatic ... of disorders of the autonomic nervous system or due to side effects of medications such as midodrine and droxidopa. Naschitz, J ...
A meta-analysis of clinical trials of midodrine or droxidopa in patients with low blood pressure when standing found that ... midodrine increased standing blood pressure more than droxidopa but that midodrine but not droxidopa increased the risk of high ... "Standing and Supine Blood Pressure Outcomes Associated With Droxidopa and Midodrine in Patients With Neurogenic Orthostatic ...
When non-pharmacological treatments for orthostatic hypotension have been exhausted, fludrocortisone, droxidopa, or midodrine ...
... droxidopa (INN) droxinavir (INN) droxypropine (INN) drozitumab (USAN) Dtic-Dome DTIC-Dome (Bayer) DTPA Duac duazomycin (INN) ...
Entacapone Tolcapone L-Phenylalanine → L-tyrosine → L-DOPA (levodopa) → dopamine L-DOPS (droxidopa) Ferrous iron (Fe2+) S- ...
C01CA22 Arbutamine C01CA23 Theodrenaline C01CA24 Epinephrine C01CA25 Amezinium metilsulfate C01CA26 Ephedrine C01CA27 Droxidopa ...
... droxidopa MeSH D12.125.837.300 - enterobactin MeSH D12.125.837.800 - phosphoserine MeSH D12.125.901.800 - phosphothreonine The ...
... droxidopa MeSH D02.092.211.215.311.560.651 - normetanephrine MeSH D02.092.211.215.311.600 - orciprenaline MeSH D02.092.211.215. ... droxidopa MeSH D02.092.311.461.484.400 - nordefrin MeSH D02.092.311.461.651 - normetanephrine MeSH D02.092.311.649 - ...
Droxidopa (3,4-dihydroxyphenylserine, 3,4-threo-DOPS, L-threo-dihydroxyphenylserine, L-threodops, Northera, threo-dopaserine, ...
  • Northera (droxidopa) is a prescription medication used to treat symptoms of neurogenic orthostatic hypotension in adults. (breathinglabs.com)
  • Also known as droxidopa, Northera works like a chemical messenger. (moneymorning.com)
  • In February 2014, the Food and Drug Administration approved droxidopa for the treatment of symptomatic neurogenic orthostatic hypotension. (wikipedia.org)
  • WASHINGTON, D.C. - The U.S. Food and Drug Administration (FDA) should not approve droxidopa, a proposed treatment of neurogenic orthostatic hypotension (NOH) - a disorder marked by feeling faint upon standing up due to a drop in blood pressure, Public Citizen said in a letter to the agency today. (citizen.org)
  • Droxidopa is prescribed to treat neurogenic orthostatic hypotension. (healthprep.com)
  • We aim to describe novel application of droxidopa, an enteral precursor of norepinephrine that is approved to treat neurogenic orthostatic hypotension, in the acute post-SCI setting. (accjournal.org)
  • Unlike norepinephrine, droxidopa is capable of crossing the protective blood-brain barrier (BBB). (wikipedia.org)
  • Droxidopa is a prodrug of norepinephrine used to increase the concentrations of these neurotransmitters in the body and brain. (wikipedia.org)
  • Droxidopa works by increasing the levels of norepinephrine in the peripheral nervous system (PNS), thus enabling the body to maintain blood flow upon and while standing. (wikipedia.org)
  • Droxidopa can also cross the blood-brain barrier (BBB) where it is converted to norepinephrine from within the brain. (wikipedia.org)
  • Droxidopa can be coupled with a peripheral aromatic L-amino acid decarboxylase inhibitor (AAADI) or DOPA decarboxylase inhibitor (DDC) such as carbidopa (Lodosyn) to increase central norepinephrine concentrations while minimizing increases of peripheral levels. (wikipedia.org)
  • Whereas levodopa functions as a precursor and prodrug to dopamine, droxidopa is a precursor and prodrug of norepinephrine. (wikipedia.org)
  • however, droxidopa is directly metabolized to norepinephrine. (affygility.com)
  • A systematic review and meta-analysis conducted on clinical trials comparing the clinical use of droxidopa and midodrine have found that midodrine was more likely to cause supine hypertension than droxidopa in patients with NOH. (wikipedia.org)
  • Droxidopa has a mechanism similar to that of midodrine but a longer duration of action. (msdmanuals.com)
  • Commonly used in conjunction with a drug that increases blood vessel constriction, such as midodrine, droxidopa or other agents. (msadownunder.org.au)
  • Droxidopa may be an alternative enteral therapy for those intolerant of midodrine due to reflex bradycardia. (accjournal.org)
  • We describe two patients suffering traumatic cervical SCI who were successfully weaned off IV vasopressors with droxidopa after failing with midodrine. (accjournal.org)
  • However, with the addition of droxidopa, this was avoided, and the patient was weaned off IV vasopressors on dual oral therapy with midodrine and droxidopa. (accjournal.org)
  • Droxidopa may be a viable enteral therapy to treat hypotension in patients after acute SCI who are otherwise not tolerating midodrine in order to wean off IV vasopressors. (accjournal.org)
  • citation needed] Droxidopa was developed by Sumitomo Pharmaceuticals for the treatment of hypotension, including NOH, and NOH associated with various disorders such as MSA, FAP, and PD, as well as IDH. (wikipedia.org)
  • Following a merger with Dainippon Pharmaceuticals in 2006, Dainippon Sumitomo Pharma licensed droxidopa to Chelsea Therapeutics to develop and market it worldwide except in Japan, Korea, China, and Taiwan. (wikipedia.org)
  • Chelsea Therapeutics obtained orphan drug status (ODS) for droxidopa in the US for NOH, and that of which associated with PD, PAF, and MSA. (wikipedia.org)
  • In 2014, Chelsea Therapeutics was acquired by Lundbeck along with the rights to droxidopa which was launched in the US in Sept 2014. (wikipedia.org)
  • In 2012, following review of the original new drug application submitted by Chelsea Therapeutics, the FDA concluded that droxidopa should not be approved because data from three randomized controlled studies had shown a lack of evidence that the medication was effective. (citizen.org)
  • As droxidopa is a prodrug for noradrenaline, its effects will be through noradrenaline activation of adrenoceptors. (guidetopharmacology.org)
  • These treatments include treating mice with droxidopa, a compound similar to the Parkinson's drug levodopa, but which is converted to noradrenaline rather than dopamine. (uic.edu)
  • Objectives: To determine the effect of an escalating dose of droxidopa (100, 200, and 400mg) compared with placebo on seated blood pressure (BP) in hypotensive individuals with spinal cord injury (SCI). (mssm.edu)
  • Freezing of gait in Parkinson's disease (off-label) With over 20 years on the market, droxidopa has proven to have few side effects of which most are mild. (wikipedia.org)
  • Droxidopa is used to treat dizziness, light-headedness, or fainting sensation and a sudden fall in blood pressure caused by several diseases, including Parkinson's. (affygility.com)
  • Conclusions: Our preliminary findings suggest that droxidopa, at the doses tested, does not cause excessive increases in supine BP and the 400-mg dose appears to be effective at increasing seated BP for up to 3 hours in persons with SCI. (mssm.edu)
  • oxymetazoline topical and droxidopa both increase sympathetic (adrenergic) effects, including increased blood pressure and heart rate. (medscape.com)
  • Droxidopa alone and in combination with carbidopa has been studied in the treatment of attention deficit hyperactivity disorder (ADHD). (wikipedia.org)
  • Treatment with droxidopa facilitated rapidly weaning IV vasopressors and transfer to a lower level of care within 72 hours of treatment initiation. (accjournal.org)
  • Increase in supine BP was not worsened following droxidopa, and the expected fall in BP when transferred to the seated position was prevented with droxidopa 200 and 400mg. (mssm.edu)
  • Results: Seated BP was significantly elevated with 400mg droxidopa compared with placebo and 100mg droxidopa for 3 hours and was elevated for 2 hours compared with 200mg droxidopa. (mssm.edu)
  • In February 2014, the Food and Drug Administration approved droxidopa for the treatment of symptomatic neurogenic orthostatic hypotension. (wikipedia.org)
  • Droxidopa is used to treat symptoms (dizziness, lightheadedness, or a fainting sensation [feeling that you are about to black out]) of neurogenic orthostatic hypotension (a sudden fall in blood pressure that occurs when a person assumes a standing position caused by certain nervous system conditions). (medlineplus.gov)
  • Cite this: FDA Clears Droxidopa for Neurogenic Orthostatic Hypotension - Medscape - Feb 18, 2014. (medscape.com)
  • Droxidopa is being developed by Chelsea Therapeutics for treating symptomatic, neurogenic orthostatic hypotension in patients with primary autonomic failure -- which can be associated with Parkinson's disease and multiple system atrophy -- dopamine beta-hydroxylase deficiency, and nondiabetic autonomic neuropathy. (medpagetoday.com)
  • Droxidopa is an orally available prodrug of norepinephrine that is used in the treatment of symptomatic orthostatic hypotension due to neurogenic causes of autonomic failure. (nih.gov)
  • Droxidopa: a review of its use in symptomatic neurogenic orthostatic hypotension. (nih.gov)
  • Randomized withdrawal study of patients with symptomatic neurogenic orthostatic hypotension responsive to droxidopa. (nih.gov)
  • Droxidopa and Reduced Falls in a Trial of Parkinson Disease Patients With Neurogenic Orthostatic Hypotension. (nih.gov)
  • In a letter to the Food and Drug Administration (FDA) Public Citizen urges the agency to not approve the new drug application for droxidopa for treatment of patients with neurogenic orthostatic hypotension. (citizen.org)
  • Droxidopa capsules are indicated for the treatment of orthostatic dizziness, lightheadedness, or the "feeling that you are about to black out" in adult patients with symptomatic neurogenic orthostatic hypotension (nOH) caused by primary autonomic failure (Parkinson's disease [PD], multiple system atrophy, and pure autonomic failure), dopamine beta-hydroxylase deficiency, and non-diabetic autonomic neuropathy. (nih.gov)
  • But last month droxidopa was denied approval by the Food and Drug Administration (FDA) to treat orthostatic hypotension (a sudden drop in blood pressure when standing up) for people with PD and several other neurological disorders. (michaeljfox.org)
  • The FDA notes that the effectiveness of droxidopa was shown through 2 weeks in 2 clinical trials in patients with NOH. (medscape.com)
  • The continued effectiveness of droxidopa capsules should be assessed periodically ( 1 ). (nih.gov)
  • Droxidopa may cause or worsen supine hypertension (high blood pressure that occurs when lying flat on your back) that may increase the risk of cardiovascular events such as heart attack and stroke. (medlineplus.gov)
  • You should raise the head of your bed when resting or sleeping and take droxidopa at least 3 hours before bedtime to reduce the risk of supine hypertension. (medlineplus.gov)
  • The FDA says droxidopa will carry a boxed warning about the risk for supine hypertension. (medscape.com)
  • Secondarily, we aimed to determine the effect of droxidopa on (1) supine BP and heart rate, (2) the change in BP and heart rate when these individuals were transferred from the supine to the seated position, and (3) adverse event (AE) reporting. (mssm.edu)
  • Increase in supine BP was not worsened following droxidopa, and the expected fall in BP when transferred to the seated position was prevented with droxidopa 200 and 400mg. (mssm.edu)
  • Conclusions: Our preliminary findings suggest that droxidopa, at the doses tested, does not cause excessive increases in supine BP and the 400-mg dose appears to be effective at increasing seated BP for up to 3 hours in persons with SCI. (mssm.edu)
  • The most common adverse events reported by clinical trial participants taking droxidopa were headache, dizziness, nausea, hypertension, and fatigue. (medscape.com)
  • Patients taking droxidopa reported a decrease in dizziness, lightheadedness, feeling faint, or feeling as if they might black out compared with those taking a placebo, the FDA said. (medscape.com)
  • Droxidopa comes as a capsule to take by mouth. (medlineplus.gov)
  • tell your doctor and pharmacist if you are allergic to droxidopa, aspirin, tartrazine (a yellow dye in some processed foods and medications), other medications, or any of the ingredients in the capsule. (medlineplus.gov)
  • The FDA approved droxidopa under the accelerated approval program, which allows for approval of a drug to treat a serious disease based on clinical data showing that the drug has an effect on an intermediate clinical measure (in this case, short-term relief of dizziness) that is reasonably likely to predict the outcome of ultimate interest (relief of dizziness during chronic treatment). (medscape.com)
  • Subjects underwent up to 2 weeks of double-blind titration of droxidopa or placebo, followed by 8 weeks of double-blind maintenance treatment (100-600 mg thrice-daily). (nih.gov)
  • At week 1, mean (standard deviation) improvement on OHSA item 1 was 2.3 (2.95) for droxidopa versus 1.3 (3.16) for placebo (P = 0.018). (nih.gov)
  • In addition, mean increase in s-SBP at week 1 was 6.4 (18.85) for droxidopa versus 0.7 (20.18) mmHg for placebo (nominal P value: 0.032). (nih.gov)
  • Interventions: Placebo on visit 1, droxidopa 100mg on visit 2, droxidopa 200mg on visit 3, and droxidopa 400mg on visit 4. (mssm.edu)
  • Results: Seated BP was significantly elevated with 400mg droxidopa compared with placebo and 100mg droxidopa for 3 hours and was elevated for 2 hours compared with 200mg droxidopa. (mssm.edu)
  • Increase in droxidopa intra-HD MAP were not significantly different from placebo, although droxidopa groups showed significant improvements in mean SBP after HD of +4.8 ± 11.6 mm Hg (600-mg) and +3.4 ± 13.1 (400-mg) compared with -4.4 ± 17.9 mm Hg in placebo, and the drop seen in mean nadir SBP pre- to intra-HD was also reduced. (nephronpower.com)
  • The green light follows a 16-1 vote last month in favor of approval of droxidopa for NOH from the FDA's Cardiovascular and Renal Drugs Advisory Committee, despite their concerns about lack of evidence of long-term durability, as reported previously by Medscape Medical News . (medscape.com)
  • The Committee first considered droxidopa for NOH in February 2012, and voted in a close vote of 7 to 4 in favor of approval . (medscape.com)
  • Precursor sintético de la noradrenalina que se usa en el tratamiento de los TRASTORNOS PARKINSONIANOS y de la HIPOTENSIÓN ORTOSTÁTICA. (bvsalud.org)
  • These highlights do not include all the information needed to use DROXIDOPA CAPSULES safely and effectively. (nih.gov)
  • See full prescribing information for DROXIDOPA CAPSULES. (nih.gov)
  • Given the lack of evidence that droxidopa is effective, FDA approval of the drug would undermine the integrity and meaningfulness of its own standard for approving drugs and cause immeasurable harm to the agency's reputation. (citizen.org)
  • The therapeutic efficacy of Droxidopa can be increased when used in combination with Pyrrobutamine. (drugbank.com)
  • ozanimod increases toxicity of droxidopa by sympathetic (adrenergic) effects, including increased blood pressure and heart rate. (medscape.com)
  • droxidopa will decrease the level or effect of iobenguane I 131 by Other (see comment). (medscape.com)
  • Droxidopa alone and in combination with carbidopa has been studied in the treatment of attention deficit hyperactivity disorder (ADHD). (wikipedia.org)
  • carbidopa decreases effects of droxidopa by decreasing metabolism. (medscape.com)
  • almotriptan and droxidopa both increase sympathetic (adrenergic) effects, including increased blood pressure and heart rate. (medscape.com)
  • eletriptan and droxidopa both increase sympathetic (adrenergic) effects, including increased blood pressure and heart rate. (medscape.com)
  • Excretion The mean elimination half-life of droxidopa is approximately 2.5 hours in humans. (pfeiffertheface.com)
  • Freezing of gait in Parkinson's disease (off-label) With over 20 years on the market, droxidopa has proven to have few side effects of which most are mild. (wikipedia.org)
  • Droxidopa is in a class of medications called alpha and beta-adrenergic agonists. (medlineplus.gov)

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