A potentially neurotoxic 8-hydroxyquinoline derivative long used as a topical anti-infective, intestinal antiamebic, and vaginal trichomonacide. The oral preparation has been shown to cause subacute myelo-optic neuropathy and has been banned worldwide.
The 8-hydroxy derivatives inhibit various enzymes and their halogenated derivatives, though neurotoxic, are used as topical anti-infective agents, among other uses.
Inflammation of the spinal cord. Relatively common etiologies include infections; AUTOIMMUNE DISEASES; SPINAL CORD; and ischemia (see also SPINAL CORD VASCULAR DISEASES). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction.
8-Hydroxyquinolinols chlorinated on the number 5 and/or 7 carbon atom(s). They are antibacterial, antiprotozoal, and antidiarrheal, especially in amebiasis, and have also been used as antiseborrheics. The compounds are mostly used topically, but have been used also as animal feed additives. They may cause optic and other neuropathies and are most frequently administered in combination with other agents.
A potent mutagen and carcinogen. It is a reduction product of 4-NITROQUINOLINE-1-OXIDE. It binds with nucleic acids and inactivates both bacteria and bacteriophage.
Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS.
An antiseptic with mild fungistatic, bacteriostatic, anthelmintic, and amebicidal action. It is also used as a reagent and metal chelator, as a carrier for radio-indium for diagnostic purposes, and its halogenated derivatives are used in addition as topical anti-infective agents and oral antiamebics.
Quinolines substituted in any position by one or more nitro groups.
A metallic element of atomic number 30 and atomic weight 65.38. It is a necessary trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Zinc deficiency is associated with ANEMIA, short stature, HYPOGONADISM, impaired WOUND HEALING, and geophagia. It is known by the symbol Zn.
Detection and counting of scintillations produced in a fluorescent material by ionizing radiation.
Substances used on humans and other animals that destroy harmful microorganisms or inhibit their activity. They are distinguished from DISINFECTANTS, which are used on inanimate objects.
Adverse cutaneous reactions caused by ingestion, parenteral use, or local application of a drug. These may assume various morphologic patterns and produce various types of lesions.
A group of disorders having a benign course but exhibiting clinical and histological features suggestive of malignant lymphoma. Pseudolymphoma is characterized by a benign infiltration of lymphoid cells or histiocytes which microscopically resembles a malignant lymphoma. (From Dorland, 28th ed & Stedman, 26th ed)
Rare skin eruption characterized by acute formation of pustules filled with NEUTROPHILS, fever, and peripheral blood LEUKOCYTOSIS. Most cases are associated with the use of antibiotics (e.g., BETA-LACTAMS).
Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke's disease), fifth (ERYTHEMA INFECTIOSUM), and sixth (EXANTHEMA SUBITUM) numeric designations survive as occasional synonyms in current terminology.
This drug combination has proved to be an effective therapeutic agent with broad-spectrum antibacterial activity against both gram-positive and gram-negative organisms. It is effective in the treatment of many infections, including PNEUMOCYSTIS PNEUMONIA in AIDS.
Skin diseases characterized by local or general distributions of blisters. They are classified according to the site and mode of blister formation. Lesions can appear spontaneously or be precipitated by infection, trauma, or sunlight. Etiologies include immunologic and genetic factors. (From Scientific American Medicine, 1990)
'Skin diseases' is a broad term for various conditions affecting the skin, including inflammatory disorders, infections, benign and malignant tumors, congenital abnormalities, and degenerative diseases, which can cause symptoms such as rashes, discoloration, eruptions, lesions, itching, or pain.
An enzyme that catalyzes the reversible isomerization of D-mannose-6-phosphate to form D-fructose-6-phosphate, an important step in glycolysis. EC 5.3.1.8.
One or more types of plant seed proteins providing the large amounts of AMINO ACIDS utilized in GERMINATION and SEEDLING growth. As seeds are the major food source from AGRICULTURAL CROPS, seed storage proteins are a major source of DIETARY PROTEINS.
An enzyme that catalyzes the conversion of L-CYSTEINE to 3-sulfinoalanine (3-sulfino-L-alanine) in the CYSTEINE metabolism and TAURINE and hypotaurine metabolic pathways.
Proteins found in plants (flowers, herbs, shrubs, trees, etc.). The concept does not include proteins found in vegetables for which VEGETABLE PROTEINS is available.
The encapsulated embryos of flowering plants. They are used as is or for animal feed because of the high content of concentrated nutrients like starches, proteins, and fats. Rapeseed, cottonseed, and sunflower seed are also produced for the oils (fats) they yield.
A family of histone demethylases that share a conserved Jumonji C domain. The enzymes function via an iron-dependent dioxygenase mechanism that couples the conversion of 2-oxoglutarate to succinate to the hydroxylation of N-methyl groups.
Derivatives of OXALIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that are derived from the ethanedioic acid structure.

Metal chelator decreases Alzheimer beta-amyloid plaques. (1/73)

Transgenic mice developing beta-amyloid (Abeta) plaques are advancing experimental treatment strategies for Alzheimer's disease. The metal chelator, clioquinol, is reported by Cherny et al. (2001) to reduce Abeta plaques, presumably by chelation of Abeta-associated zinc and copper. This and other recent Abeta-modulating treatment approaches are discussed.  (+info)

Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice. (2/73)

Inhibition of neocortical beta-amyloid (Abeta) accumulation may be essential in an effective therapeutic intervention for Alzheimer's disease (AD). Cu and Zn are enriched in Abeta deposits in AD, which are solubilized by Cu/Zn-selective chelators in vitro. Here we report a 49% decrease in brain Abeta deposition (-375 microg/g wet weight, p = 0.0001) in a blinded study of APP2576 transgenic mice treated orally for 9 weeks with clioquinol, an antibiotic and bioavailable Cu/Zn chelator. This was accompanied by a modest increase in soluble Abeta (1.45% of total cerebral Abeta); APP, synaptophysin, and GFAP levels were unaffected. General health and body weight parameters were significantly more stable in the treated animals. These results support targeting the interactions of Cu and Zn with Abeta as a novel therapy for the prevention and treatment of AD.  (+info)

An iron-responsive element type II in the 5'-untranslated region of the Alzheimer's amyloid precursor protein transcript. (3/73)

Iron-responsive elements (IREs) are the RNA stem loops that control cellular iron homeostasis by regulating ferritin translation and transferrin receptor mRNA stability. We mapped a novel iron-responsive element (IRE-Type II) within the 5'-untranslated region (5'-UTR) of the Alzheimer's amyloid precursor protein (APP) transcript (+51 to +94 from the 5'-cap site). The APP mRNA IRE is located immediately upstream of an interleukin-1 responsive acute box domain (+101 to +146). APP 5'-UTR conferred translation was selectively down-regulated in response to intracellular iron chelation using three separate reporter assays (chloramphenicol acetyltransferase, luciferase, and red fluorescent protein reflecting an inhibition of APP holoprotein translation in response to iron chelation. Iron influx reversed this inhibition. As an internal control to ensure specificity, a viral internal ribosome entry sequence was unresponsive to intracellular iron chelation with desferrioxamine. Using RNA mobility shift assays, the APP 5'-UTRs, encompassing the IRE, bind specifically to recombinant iron-regulatory proteins (IRP) and to IRP from neuroblastoma cell lysates. IRP binding to the APP 5'-UTR is reduced after treatment of cells with desferrioxamine and increased after interleukin-1 stimulation. IRP binding is abrogated when APP cRNA probe is mutated in the core IRE domain (Delta4 bases:Delta83AGAG86). Iron regulation of APP mRNA through the APP 5'-UTR points to a role for iron in the metabolism of APP and confirms that this RNA structure can be a target for the selection of small molecule drugs, such as desferrioxamine (Fe chelator) and clioquinol (Fe, Cu, and Zn chelator), which reduce Abeta peptide burden during Alzheimer's disease.  (+info)

Ironic fate: can a banned drug control metal heavies in neurodegenerative diseases? (4/73)

In this issue of Neuron, Kaur et al. demonstrate that iron chelation by ferritin transgene or the metal chelator clioquinol prevent oxidative damage and MPTP toxicity in mice. This raises the issue of specific iron chelators or clioquinol for control of oxidative damage in Parkinson's, Alzheimer's, and other neurodegenerative diseases, but not without safety concerns.  (+info)

Genetic or pharmacological iron chelation prevents MPTP-induced neurotoxicity in vivo: a novel therapy for Parkinson's disease. (5/73)

Studies on postmortem brains from Parkinson's patients reveal elevated iron in the substantia nigra (SN). Selective cell death in this brain region is associated with oxidative stress, which may be exacerbated by the presence of excess iron. Whether iron plays a causative role in cell death, however, is controversial. Here, we explore the effects of iron chelation via either transgenic expression of the iron binding protein ferritin or oral administration of the bioavailable metal chelator clioquinol (CQ) on susceptibility to the Parkinson's-inducing agent 1-methyl-4-phenyl-1,2,3,6-tetrapyridine (MPTP). Reduction in reactive iron by either genetic or pharmacological means was found to be well tolerated in animals in our studies and to result in protection against the toxin, suggesting that iron chelation may be an effective therapy for prevention and treatment of the disease.  (+info)

Subacute myelo-optic neuropathy and clioquinol. An epidemiological case-history for diagnosis. (6/73)

Between about 1955 and 1970, some 100,000 Japanese were diagnosed as having subacute myelooptic neuropathy (SMON), a new disease characterized by abdominal and neurological manifestations, the former nearly always preceding the latter. Circumstantial evidence obtained in 1969-70 suggested that SMON might have been caused by clioquinol (CQL), a gastrointestinal disinfectant, and led to the suspension of further sales of CQL in Japan. However, several inconsistencies for the CQL theory of SMON have now emerged; first, CQL had been widely used in Japan for nearly 20 years before SMON occurred. Secondly, the SMON epidemic began to subside several months before CQL sales were suspended. Thirdly, a large proportion of SMON patients--probably about one-third and possibly more--had not taken CQL within six months of the onset of the disease (the modal interval between first taking CQL and the onset of SMON being about three weeks, and more than 100 days in only 4% of SMON patients); of the remaining two-thirds or so, many had taken CQL as part of the treatment of the first (that is, abdominal) symptoms of SMON itself. Fourthly, there was no dose-response relationship. Finally, SMON rarely, if ever, occurred outside Japan. CQL could, however, have been involved in the causation of SMON as an optional enhancer of some other necessary cause; the history of post-war environmental pollution in Japan is compatible with this hypothesis. Over-readiness to accept postulated toxic effects of medicines and chemicals as proven is likely to do at least as much harm as good to individual and community health.  (+info)

Cu2+-induced modification of the kinetics of A beta(1-42) channels. (7/73)

We found that the amyloid beta peptide A beta(1-42) is capable of interacting with membrane and forming heterogeneous ion channels in the absence of any added Cu2+ or biological redox agents that have been reported to mediate A beta(1-42) toxicity. The A beta(1-42)-formed cation channel was inhibited by Cu2+ in cis solution ([Cu2+]cis) in a voltage- and concentration-dependent manner between 0 and 250 microM. The [Cu2+]cis-induced channel inhibition is fully reversible at low concentrations between 50 and 100 microM [Cu2+]cis and partially reversible at 250 microM [Cu2+]cis. The inhibitory effects of [Cu2+]cis between 50 and 250 microM on the channel could not be reversed with addition of Cu2+-chelating agent clioquinol (CQ) at concentrations between 64 and 384 microM applied to the cis chamber. The effects of 200-250 microM [Cu2+]cis on the burst and intraburst kinetic parameters were not fully reversible with either wash or 128 microM [CQ]cis. The kinetic analysis of the data indicate that Cu2+-induced inhibition was mediated via both desensitization and an open channel block mechanism and that Cu2+ binds to the histidine residues located at the mouth of the channel. It is proposed that the Cu2+-binding site of the A beta(1-42)-formed channels is modulated with Cu2+ in a similar way to those of channels formed with the prion protein fragment PrP(106-126), suggesting a possible common mechanism for Cu2+ modulation of A beta and PrP channel proteins linked to neurodegenerative diseases.  (+info)

Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity. (8/73)

Although the accumulation of the neurotoxic peptide beta amyloid (betaA) in the CNS is a hallmark of Alzheimer's disease, the mechanism of betaA neurotoxicity remains controversial. In cultures of mixed neurons and astrocytes, we found that both the full-length peptide betaA (1-42) and the neurotoxic fragment (25-35) caused sporadic cytoplasmic calcium [intracellular calcium ([Ca2+]c)] signals in astrocytes that continued for hours, whereas adjacent neurons were completely unaffected. Nevertheless, after 24 hr, although astrocyte cell death was marginally increased, approximately 50% of the neurons had died. The [Ca2+]c signal was entirely dependent on Ca2+ influx and was blocked by zinc and by clioquinol, a heavy-metal chelator that is neuroprotective in models of Alzheimer's disease. Neuronal death was associated with Ca2+-dependent glutathione depletion in both astrocytes and neurons. Thus, astrocytes appear to be the primary target of betaA, whereas the neurotoxicity reflects the neuronal dependence on astrocytes for antioxidant support.  (+info)

Clioquinol is an antimicrobial drug that contains a combination of clioquinal and hydrocortisone acetate. It is used topically to treat various skin infections and inflammatory conditions. Clioquinol has antibacterial and antifungal properties, while hydrocortisone acetate is a corticosteroid that reduces inflammation and suppresses the immune response.

Clioquinol was first synthesized in the 1930s and was widely used as an antidiarrheal medication until it was banned in many countries due to its association with a neurological disorder called subacute myelooptic neuropathy (SMON). However, topical clioquinol is still available in some countries for the treatment of skin conditions.

It's important to note that topical clioquinol should be used with caution and under the supervision of a healthcare professional, as it can cause skin irritation and sensitization in some individuals. Additionally, prolonged or excessive use of corticosteroids like hydrocortisone acetate can lead to thinning of the skin, increased susceptibility to infection, and other adverse effects.

Hydroxyquinolines are a group of synthetic antimicrobial agents that contain a hydroxyl group (-OH) attached to a quinoline ring. They have been used in the treatment of various bacterial, fungal, and parasitic infections. Some common examples of hydroxyquinolines include chloroquine, hydroxychloroquine, and quinacrine. These agents work by inhibiting the growth and multiplication of microorganisms, although their exact mechanisms of action may vary. Chloroquine and hydroxychloroquine, for example, are known to interfere with the replication of the malaria parasite within red blood cells, while quinacrine has been used to treat certain types of protozoal infections.

It is important to note that the use of hydroxyquinolines is associated with a number of potential side effects and risks, including gastrointestinal disturbances, visual disturbances, and cardiac toxicity. As such, they should only be used under the close supervision of a healthcare professional.

Myelitis is a medical term that refers to inflammation of the spinal cord. This inflammation can cause damage to the myelin sheath, which is the protective covering of nerve fibers in the spinal cord. As a result, the transmission of nerve impulses along the spinal cord may be disrupted, leading to various neurological symptoms.

Myelitis can affect any part of the spinal cord and can have many different causes, including infections (such as viral or bacterial infections), autoimmune disorders (such as multiple sclerosis), and other conditions (such as spinal cord injuries or tumors). The specific symptoms of myelitis depend on the location and severity of the inflammation. They may include muscle weakness, numbness or tingling sensations, pain, bladder or bowel dysfunction, and difficulty with coordination and balance.

Myelitis can be a serious condition that requires prompt medical attention and treatment. Treatment typically focuses on addressing the underlying cause of the inflammation, as well as managing symptoms and supporting recovery.

Chloroquinolinols are a class of chemical compounds that contain a quinoline ring substituted with a chlorine atom and a hydroxy or alkoxy group. These compounds have various medical applications, particularly in the treatment of parasitic diseases such as malaria. Chloroquine is one of the most well-known chloroquinolinols, which has been widely used as an antimalarial drug for many years. Other examples of chloroquinolinols include hydroxychloroquine and chloroxynol. These compounds have anti-inflammatory, antimicrobial, and antiviral properties, making them useful in the treatment of a variety of medical conditions. However, they can also have side effects and potential toxicity, so their use must be carefully monitored and managed by healthcare professionals.

4-Hydroxyaminoquinoline-1-oxide, also known as 4HAQ or acriflavine hydroxylamine, is a chemical compound that has been used in research to study the mechanisms of DNA damage and mutagenesis. It is an aromatic heterocyclic amine and is known to be a potent mutagen and carcinogen.

The compound works by forming adducts with DNA, particularly at guanine residues, leading to mispairing during replication and the introduction of mutations. It has been used as a tool in molecular biology to study the effects of DNA damage on cellular processes such as transcription, replication, and repair.

It is important to note that 4HAQ is not used clinically in medicine due to its toxicity and carcinogenic properties.

Chelating agents are substances that can bind and form stable complexes with certain metal ions, preventing them from participating in chemical reactions. In medicine, chelating agents are used to remove toxic or excessive amounts of metal ions from the body. For example, ethylenediaminetetraacetic acid (EDTA) is a commonly used chelating agent that can bind with heavy metals such as lead and mercury, helping to eliminate them from the body and reduce their toxic effects. Other chelating agents include dimercaprol (BAL), penicillamine, and deferoxamine. These agents are used to treat metal poisoning, including lead poisoning, iron overload, and copper toxicity.

I'm sorry for any confusion, but "Oxyquinoline" does not have a specific medical definition as it is not a widely recognized medical term or a medication used in human healthcare. Oxyquinoline is an organic compound that contains a quinoline ring substituted with an alcohol group (hydroxyl) at position 8. It has been used in the past as a disinfectant and antiseptic, but it's not common in modern medical practice.

If you have any questions about medical terminology or concepts, please provide more context so I can offer a more accurate and helpful response.

I'm sorry for any confusion, but "Nitroquinolines" is not a recognized term in medical or pharmacological sciences. It seems to be a chemical category that consists of compounds containing a quinoline nucleus (a heterocyclic aromatic compound) with one or more nitro groups attached to it.

Quinoline derivatives have been explored for their potential medicinal properties, including antimalarial and antibacterial activities. However, the term "Nitroquinolines" does not specifically refer to a medical definition or a particular therapeutic application. If you're looking for information on specific quinoline-based compounds with nitro groups, I would be happy to help if you could provide more context or details.

Zinc is an essential mineral that is vital for the functioning of over 300 enzymes and involved in various biological processes in the human body, including protein synthesis, DNA synthesis, immune function, wound healing, and cell division. It is a component of many proteins and participates in the maintenance of structural integrity and functionality of proteins. Zinc also plays a crucial role in maintaining the sense of taste and smell.

The recommended daily intake of zinc varies depending on age, sex, and life stage. Good dietary sources of zinc include red meat, poultry, seafood, beans, nuts, dairy products, and fortified cereals. Zinc deficiency can lead to various health problems, including impaired immune function, growth retardation, and developmental delays in children. On the other hand, excessive intake of zinc can also have adverse effects on health, such as nausea, vomiting, and impaired immune function.

Scintillation counting is a method used in medical physics and nuclear medicine to detect and quantify radioactivity. It relies on the principle that certain materials, known as scintillators, emit light flashes (scintillations) when they absorb ionizing radiation. This light can then be detected and measured to determine the amount of radiation present.

In a scintillation counting system, the sample containing radioisotopes is placed in close proximity to the scintillator. When radiation is emitted from the sample, it interacts with the scintillator material, causing it to emit light. This light is then detected by a photomultiplier tube (PMT), which converts the light into an electrical signal that can be processed and counted by electronic circuits.

The number of counts recorded over a specific period of time is proportional to the amount of radiation emitted by the sample, allowing for the quantification of radioactivity. Scintillation counting is widely used in various applications such as measuring radioactive decay rates, monitoring environmental radiation levels, and analyzing radioisotopes in biological samples.

Anti-infective agents, local, are medications that are applied directly to a specific area of the body to prevent or treat infections caused by bacteria, fungi, viruses, or parasites. These agents include topical antibiotics, antifungals, antivirals, and anti-parasitic drugs. They work by killing or inhibiting the growth of the infectious organisms, thereby preventing their spread and reducing the risk of infection. Local anti-infective agents are often used to treat skin infections, eye infections, and other localized infections, and can be administered as creams, ointments, gels, solutions, or drops.

A "drug eruption" is a general term used to describe an adverse skin reaction that occurs as a result of taking a medication. These reactions can vary in severity and appearance, and may include symptoms such as rash, hives, itching, redness, blistering, or peeling of the skin. In some cases, drug eruptions can also cause systemic symptoms such as fever, fatigue, or joint pain.

The exact mechanism by which drugs cause eruptions is not fully understood, but it is thought to involve an abnormal immune response to the medication. There are many different types of drug eruptions, including morphilliform rashes, urticaria (hives), fixed drug eruptions, and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), which is a severe and potentially life-threatening reaction.

If you suspect that you are experiencing a drug eruption, it is important to seek medical attention promptly. Your healthcare provider can help determine the cause of the reaction and recommend appropriate treatment. In some cases, it may be necessary to discontinue the medication causing the reaction and switch to an alternative therapy.

Pseudolymphoma is a term used to describe a benign reactive lymphoid hyperplasia that mimics the clinical and histopathological features of malignant lymphomas. It is also known as pseudolymphomatous cutis or reactive lymphoid hyperplasia.

Pseudolymphoma can occur in various organs, but it is most commonly found in the skin. It is usually caused by a localized immune response to an antigenic stimulus such as insect bites, tattoos, radiation therapy, or certain medications. The condition presents as a solitary or multiple nodular lesions that may resemble lymphoma both clinically and histologically.

Histologically, pseudolymphoma is characterized by a dense infiltrate of lymphocytes, plasma cells, and other immune cells, which can mimic the appearance of malignant lymphoma. However, unlike malignant lymphomas, pseudolymphomas lack cytological atypia, mitotic activity, and clonal proliferation of lymphoid cells.

Pseudolymphoma is usually a self-limiting condition that resolves spontaneously or with the removal of the antigenic stimulus. However, in some cases, it may persist or recur, requiring further evaluation and treatment to exclude malignant lymphoma.

Acute Generalized Exanthematous Pustulosis (AGEP) is a severe cutaneous adverse reaction that typically occurs within 48 hours after the initiation of medication. It is characterized by the rapid development of widespread sterile pustules on an erythematous and edematous base, often accompanied by systemic symptoms such as fever and neutrophilia.

The most common triggers for AGEP are antibiotics (such as beta-lactams, macrolides, and fluoroquinolones), antifungals, and calcium channel blockers. The diagnosis of AGEP is based on clinical presentation, histopathological findings, and the exclusion of other causes of pustular eruptions.

The management of AGEP includes immediate discontinuation of the offending medication, supportive care, and sometimes systemic corticosteroids. The prognosis is generally good with most patients recovering within 2 weeks, although recurrences may occur upon re-exposure to the causative agent.

An exanthem is a skin eruption or rash that often occurs as a symptom of various diseases, such as infectious illnesses. It can appear in different forms, including maculopapular (consisting of both macules and papules), vesicular (small fluid-filled blisters), petechial (small purple or red spots caused by bleeding under the skin), or erythematous (reddened). The rash can be localized to certain areas of the body or generalized, covering large parts or the entire body. Exanthems are usually accompanied by other symptoms related to the underlying disease, such as fever, cough, or muscle aches.

Trimethoprim-sulfamethoxazole combination is an antibiotic medication used to treat various bacterial infections. It contains two active ingredients: trimethoprim and sulfamethoxazole, which work together to inhibit the growth of bacteria by interfering with their ability to synthesize folic acid, a vital component for their survival.

Trimethoprim is a bacteriostatic agent that inhibits dihydrofolate reductase, an enzyme needed for bacterial growth, while sulfamethoxazole is a bacteriostatic sulfonamide that inhibits the synthesis of tetrahydrofolate by blocking the action of the enzyme bacterial dihydropteroate synthase. The combination of these two agents produces a synergistic effect, increasing the overall antibacterial activity of the medication.

Trimethoprim-sulfamethoxazole is commonly used to treat urinary tract infections, middle ear infections, bronchitis, traveler's diarrhea, and pneumocystis pneumonia (PCP), a severe lung infection that can occur in people with weakened immune systems. It is also used as a prophylactic treatment to prevent PCP in individuals with HIV/AIDS or other conditions that compromise the immune system.

As with any medication, trimethoprim-sulfamethoxazole combination can have side effects and potential risks, including allergic reactions, skin rashes, gastrointestinal symptoms, and blood disorders. It is essential to follow the prescribing physician's instructions carefully and report any adverse reactions promptly.

Vesiculobullous skin diseases are a group of disorders characterized by the formation of blisters (vesicles) and bullae (larger blisters) on the skin. These blisters form when there is a separation between the epidermis (outer layer of the skin) and the dermis (layer beneath the epidermis) due to damage in the area where they join, known as the dermo-epidermal junction.

There are several types of vesiculobullous diseases, each with its own specific causes and symptoms. Some of the most common types include:

1. Pemphigus vulgaris: an autoimmune disorder where the immune system mistakenly attacks proteins that help to hold the skin together, causing blisters to form.
2. Bullous pemphigoid: another autoimmune disorder, but in this case, the immune system attacks a different set of proteins, leading to large blisters and inflammation.
3. Dermatitis herpetiformis: a skin condition associated with celiac disease, where gluten ingestion triggers an immune response that leads to the formation of itchy blisters.
4. Pemphigoid gestationis: a rare autoimmune disorder that occurs during pregnancy and causes blisters on the abdomen and other parts of the body.
5. Epidermolysis bullosa: a group of inherited disorders where there is a fragile skin structure, leading to blistering and wound formation after minor trauma or friction.

Treatment for vesiculobullous diseases depends on the specific diagnosis and may include topical or systemic medications, such as corticosteroids, immunosuppressants, or antibiotics, as well as wound care and prevention of infection.

Skin diseases, also known as dermatological conditions, refer to any medical condition that affects the skin, which is the largest organ of the human body. These diseases can affect the skin's function, appearance, or overall health. They can be caused by various factors, including genetics, infections, allergies, environmental factors, and aging.

Skin diseases can present in many different forms, such as rashes, blisters, sores, discolorations, growths, or changes in texture. Some common examples of skin diseases include acne, eczema, psoriasis, dermatitis, fungal infections, viral infections, bacterial infections, and skin cancer.

The symptoms and severity of skin diseases can vary widely depending on the specific condition and individual factors. Some skin diseases are mild and can be treated with over-the-counter medications or topical creams, while others may require more intensive treatments such as prescription medications, light therapy, or even surgery.

It is important to seek medical attention if you experience any unusual or persistent changes in your skin, as some skin diseases can be serious or indicative of other underlying health conditions. A dermatologist is a medical doctor who specializes in the diagnosis and treatment of skin diseases.

Mannose-6-Phosphate Isomerase (MPI) is an enzyme that catalyzes the interconversion between mannose-6-phosphate and fructose-6-phosphate, which are both key metabolites in the glycolysis and gluconeogenesis pathways. This enzyme plays a crucial role in maintaining the balance between these two metabolic pathways, allowing cells to either break down or synthesize glucose depending on their energy needs.

The gene that encodes for MPI is called MPI1 and is located on chromosome 4 in humans. Defects in this gene can lead to a rare genetic disorder known as Mannose-6-Phosphate Isomerase Deficiency or Congenital Disorder of Glycosylation Type IIm, which is characterized by developmental delay, intellectual disability, seizures, and various other neurological symptoms.

Seed storage proteins are a group of proteins that accumulate in the seeds of plants during their development and serve as a source of nitrogen, sulfur, and energy for the germinating embryo. They are typically rich in certain amino acids, such as proline, glutamine, and arginine, and are classified into several types based on their solubility properties.

The main types of seed storage proteins include:

1. Albumins: These are water-soluble proteins that are present in the embryo of the seed.
2. Globulins: These are salt-soluble proteins that are found in protein bodies within the seed's endosperm. They are further classified into two types, 11S and 7S globulins, based on their sedimentation coefficients.
3. Prolamins: These are alcohol-soluble proteins that are also found in the endosperm of seeds. They are rich in proline and glutamine and are often referred to as "storage proteins" because they constitute a significant portion of the seed's protein content. Examples include zein in corn, gliadin in wheat, and hordein in barley.
4. Glutelins: These are acid- or alkali-soluble proteins that are also found in the endosperm of seeds. They are typically insoluble in water, salt, and alcohol.

Seed storage proteins have important nutritional and agricultural significance. For example, they are a major source of protein for human consumption and animal feed, and their composition can affect the nutritional quality and processing properties of cereal grains and legumes. Additionally, seed storage proteins have been studied as potential allergens and as targets for genetic modification in crop plants to improve their nutritional value and yield.

Cysteine dioxygenase (CDO) is an enzyme that catalyzes the conversion of the amino acid L-cysteine to L-cysteinesulfinic acid, which is the first step in the catabolism of L-cysteine. This reaction also generates molecular oxygen as a byproduct. CDO plays important roles in various biological processes such as neurotransmitter biosynthesis and oxidative stress response. It exists as two isoforms, CDO1 and CDO2, which are encoded by separate genes and have distinct tissue distributions and functions.

"Plant proteins" refer to the proteins that are derived from plant sources. These can include proteins from legumes such as beans, lentils, and peas, as well as proteins from grains like wheat, rice, and corn. Other sources of plant proteins include nuts, seeds, and vegetables.

Plant proteins are made up of individual amino acids, which are the building blocks of protein. While animal-based proteins typically contain all of the essential amino acids that the body needs to function properly, many plant-based proteins may be lacking in one or more of these essential amino acids. However, by consuming a variety of plant-based foods throughout the day, it is possible to get all of the essential amino acids that the body needs from plant sources alone.

Plant proteins are often lower in calories and saturated fat than animal proteins, making them a popular choice for those following a vegetarian or vegan diet, as well as those looking to maintain a healthy weight or reduce their risk of chronic diseases such as heart disease and cancer. Additionally, plant proteins have been shown to have a number of health benefits, including improving gut health, reducing inflammation, and supporting muscle growth and repair.

In medical terms, "seeds" are often referred to as a small amount of a substance, such as a radioactive material or drug, that is inserted into a tissue or placed inside a capsule for the purpose of treating a medical condition. This can include procedures like brachytherapy, where seeds containing radioactive materials are used in the treatment of cancer to kill cancer cells and shrink tumors. Similarly, in some forms of drug delivery, seeds containing medication can be used to gradually release the drug into the body over an extended period of time.

It's important to note that "seeds" have different meanings and applications depending on the medical context. In other cases, "seeds" may simply refer to small particles or structures found in the body, such as those present in the eye's retina.

Jumonji domain-containing histone demethylases (JHDMs) are a family of enzymes that are responsible for removing methyl groups from specific residues on histone proteins. These enzymes play crucial roles in the regulation of gene expression by modifying the chromatin structure and influencing the accessibility of transcription factors to DNA.

JHDMs contain a conserved Jumonji C (JmjC) domain, which is responsible for their demethylase activity. They are classified into two main groups based on the type of methyl group they remove: lysine-specific demethylases (KDMs) and arginine-specific demethylases (RDMs).

KDMs can be further divided into several subfamilies, including KDM2/7, KDM3, KDM4, KDM5, and KDM6, based on their substrate specificity and the number of methyl groups they remove. For example, KDM4 enzymes specifically demethylate di- and tri-methylated lysine 9 and lysine 36 residues on histone H3, while KDM5 enzymes target mono-, di-, and tri-methylated lysine 4 residues on histone H3.

RDMs, on the other hand, are responsible for demethylating arginine residues on histones, including symmetrically or asymmetrically dimethylated arginine 2, 8, 17, and 26 residues on histone H3 and H4.

Dysregulation of JHDMs has been implicated in various human diseases, including cancer, neurological disorders, and cardiovascular diseases. Therefore, understanding the functions and regulation of JHDMs is essential for developing novel therapeutic strategies to treat these diseases.

Oxalates, also known as oxalic acid or oxalate salts, are organic compounds that contain the functional group called oxalate. Oxalates are naturally occurring substances found in various foods such as spinach, rhubarb, nuts, and seeds. They can also be produced by the body as a result of metabolism.

In the body, oxalates can bind with calcium and other minerals to form crystals, which can accumulate in various tissues and organs, including the kidneys. This can lead to the formation of kidney stones, which are a common health problem associated with high oxalate intake or increased oxalate production in the body.

It is important for individuals with a history of kidney stones or other kidney problems to monitor their oxalate intake and limit consumption of high-oxalate foods. Additionally, certain medical conditions such as hyperoxaluria, a rare genetic disorder that causes increased oxalate production in the body, may require medical treatment to reduce oxalate levels and prevent complications.

"Manufacturers of Clioquinol". DNS Fine Chemicals. 2016-01-06. Retrieved 23 December 2017. Herlekar O. "Clioquinol manufacturers ... The zinc ionophore clioquinol was shown in mice to restore zinc levels and stop the growth of prostate tumors. Research at UCSF ... Clioquinol's use as an antiprotozoal drug has been restricted or discontinued in some countries due to an event in Japan where ... Clioquinol is a constituent of the prescription medicine Vioform, which is a topical antifungal treatment. It is also used in ...
Clioquinol and PBT2 are 8-hydroxyquinoline derivatives.[citation needed] Clioquinol has antiprotozoal and topical antifungal ... Clioquinol and PBT2 are currently being studied for neurodegenerative diseases, such as Alzheimer's disease, Huntington's ...
Clioquinol, an antifungal drug and antiprotozoal drug. PBT2 QUPIC Ionophore Trace metal detection test Albert, A.; Phillips, J ...
Clioquinol was marketed as a prophylaxis to tourist diarrhoea. Dr. Olle Hansson was in the front line, fighting for a ban of ... On August 3, 1978, the Tokyo District Court ruled that the cause of SMON is Clioquinol. Its manufacturer, Ciba-Geigy, has ... and Clioquinol: Nationwide Survey", The Lancet, V301, I7796, January 27, 1973, pp. 171-173 Reisaku Kono, "The S.M.O.N. Virus ... clioquinol. Doctors in many countries boycotted Ciba-Geigy for many years. Not until 1985 was the pharmaceutical withdrawn. Dr ...
Clioquinol Coal tar Copper(II) sulfate Crystal violet - a triarylmethane dye. It has antibacterial, antifungal, and ...
Daniel, Kenyon G; Chen, Di; Orlu, Shirley; Cui, Qiuzhi; Miller, Fred R; Dou, Q Ping (2005). "Clioquinol and pyrrolidine ...
... has been shown to be more cytotoxic to HL60, DHL-4, PANC-1, and A2780 [zh] cells lines than clioquinol and other 8- ... Because the zinc chelating action of clioquinol has been associated with subacute myelo-optic neuropathy, the use of ... is more a potent anti-cancer agent than clioquinol (5-chloro-7-iodo-8-quinoline)". Cancer Letters. 312 (1): 11-17. doi:10.1016/ ...
... study of novel green UV-spectrophotometric platforms for simultaneous rapid analysis of flumethasone pivalate and clioquinol in ...
Clioquinol (Entero-vioform) was noted as successful in treatment of Blastocystis infection but removed from the market ...
Topical ketanserin seems to have a better effect on ulcer healing than clioquinol cream or zinc paste, but the evidence for ...
It is a second-generation 8-hydroxyquinoline analog intended to be a successor to clioquinol and a potential treatment of ...
It is available in combination with clioquinol, under the brand name Locacorten-Vioform (in some countries Locorten-Vioform), ...
... may refer to: Cortin, a synonym for corticosteroid Cortin, a trade name for the antifungal drug clioquinol This ...
2001: Showed that AD pathology in transgenic mice could be ameliorated by a zinc-copper chelator, clioquinol (PBT1) 2003: ... Clioquinol (PBT1) successful in a phase 2 AD clinical trial. 2003: Discovered that apoptosis and caspase activation induces ...
... may stand for: Subacute myelo-optic neuropathy, an epidemic in Japan caused by clioquinol SMON, a set of MIB extensions ...
... combinations G01AB01 Acetarsol G01AC01 Diiodohydroxyquinoline G01AC02 Clioquinol G01AC03 Chlorquinaldol G01AC05 Dequalinium ...
... clioquinol MeSH D03.438.810.350.625.420 - iodoquinol MeSH D03.438.810.350.700 - procaterol MeSH D03.438.810.410 - mefloquine ...
P01AA01 Broxyquinoline P01AA02 Clioquinol P01AA04 Chlorquinaldol P01AA05 Tilbroquinol P01AA30 Tilbroquinol and tiliquinol ... P01AA52 Clioquinol, combinations P01AB01 Metronidazole P01AB02 Tinidazole P01AB03 Ornidazole P01AB04 Azanidazole P01AB05 ...
Clioquinol and other halogenated derivatives of oxyquinoline for human internal use except or when being used solely for ...
... combinations D08AH01 Dequalinium D08AH02 Chlorquinaldol D08AH03 Oxyquinoline D08AH30 Clioquinol D08AJ01 Benzalkonium D08AJ02 ...
D09AA06 Triclosan D09AA07 Cetylpyridinium D09AA08 Aluminium chlorohydrate D09AA09 Povidone-iodine D09AA10 Clioquinol D09AA11 ...
... clioquinol (INN) clioxanide (INN) cliprofen (INN) cliropamine (INN) Clistin clobazam (INN) clobenoside (INN) clobenzepam (INN) ...
S02AA01 Chloramphenicol S02AA02 Nitrofural S02AA03 Boric acid S02AA04 Aluminium acetotartrate S02AA05 Clioquinol S02AA06 ...
"Manufacturers of Clioquinol". DNS Fine Chemicals. 2016-01-06. Retrieved 23 December 2017. Herlekar O. "Clioquinol manufacturers ... The zinc ionophore clioquinol was shown in mice to restore zinc levels and stop the growth of prostate tumors. Research at UCSF ... Clioquinols use as an antiprotozoal drug has been restricted or discontinued in some countries due to an event in Japan where ... Clioquinol is a constituent of the prescription medicine Vioform, which is a topical antifungal treatment. It is also used in ...
For ring worm. Brand Name(s): Ala-Quin. Generic Name: Clioquinol/Hydrocortisone.
Cream; Topical; Betamethasone Valerate 0.061%; Chlorocresol 0.1%; Clioquinol 1%; Gentamicin 0.1%; Tolnaftate 1%. ...
Send a request for the purchase of a pharmaceutical substance Clioquinol ...
buy Betamethasone Valerate 0.1% / Clioquinol 3% Cream 30g online at discounted rate UK - Chemist.net ... Clioquinol 3% Cream 30g buy online at £79, pharmacy UK offers prescriptions products at discounted prices. ... Betamethasone Valerate 0.1% / Clioquinol 3% Cream 30g is a Prescription Only Medicine. To purchase this item you must have a ...
... , Durham, NC. ... Hyperbaric oxygen therapy for peripheral nerve damage induced in rabbits with clioquinol.. Jun 1, 1975 , Peripheral Neuropathy ... Hyperbaric oxygen therapy for peripheral nerve damage induced in rabbits with clioquinol. Experimental neurology, 1975 Jun;47(3 ...
Be the first to review "Betnovate C (Betamethasone/Clioquinol)" Cancel reply. You must be logged in to post a review. ... Betnovate C (Betamethasone/Clioquinol). Betnovate S (Betamethasone/Salicylic)Prilox Cream (Prilocaine/Lidocaine) ... Betnovate C (Betamethasone/Clioquinol). Thumbnail. Pack Size. Per Pill. Price. Quantity. Order. ...
Adverse reactions to medications are common and often manifest as a cutaneous eruption. Drug-induced cutaneous disorders frequently display a characteristic clinical morphology such as morbilliform exanthem, urticaria, hypersensitivity syndrome, pseudolymphoma, photosensitivity, pigmentary changes, acute generalized exanthematous pustulosis, ...
SYN: chloriodoquin, clioquinol. iodochlorol (i′o-do-klor′ol). SYN: chloriodized oil. iododerma (i-o′do-der′ma). 1An eruption of ...
Clioquinol. *Copper chelation. *Next generation multifunctional chelating agents for AD. *Secretase modulators ...
Clioquinol) and diiodohydroxyquin (II) (iodoquinol). The proposed method depends on the formation of Pd II-ligand complexes in ... Clioquinol) and diiodohydroxyquin (II) (iodoquinol). The proposed method depends on the formation of Pd II-ligand complexes in ...
Vioform®see Clioquinol Topical. *Viokace®see Pancrelipase. *Viracept®see Nelfinavir. *Viramune®see Nevirapine ...
clioquinol - hydrocortisone (Vioform Hydrocortisone) * clobazam (Apo-Clobazam, Clobazam-10, Dom-Clobazam, Frisium, Novo- ...
A Better Clioquinol to Enter Phase 2. Clioquinol is a former antibiotic with a storied history. It has served to prove the ... Side-Reactions Sideswipe Clioquinol-Prevent Clinical Trial 11 Apr 2005. * Madrid: Clinical Trials Update-Where Do Things Stand? ... In Madrid, Bush reported that PBT2, Pranas second-generation compound, is an 8-hydoxyquinoline that outdoes clioquinol on a ... Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer ...
clioquinol S02AA06 hydrogen peroxide S02AA07 neomycin S02AA08 tetracycline S02AA09 chlorhexidine S02AA10 acetic acid ...
... clioquinol in 288 patients in the Philippines resulted in a better efficacy for the diflucortolone preparation in the 80 ...
Flumetasone/Clioquinol * Hydrocortisone/Gentamicin Ear Drops (Hydrocortisone) * Otomize (Dexamethasone) * Otosporin ( ...
shown that clioquinol (CQ) had therapeutic benefits in a monkey model of PD by activating the AKT serine/threonine kinase 1 ( ... Clioquinol improves motor and non-motor deficits in MPTP-induced monkey model of Parkinsons disease through AKT/mTOR pathway. ...
When AD patients were treated with clioquinol, the placebo group deteriorated faster than the clioquinol group suggesting a ... Schafer S, Pajonk FG, Multhaup G, Bayer TA (2007) Copper and clioquinol treatment in young APP transgenic and wild-type mice: ... 2003). This could be due to clioquinol mediating Cu uptake into the cell or the metal-protein-attenuating-compunds properties. ... 2001) showed that clioquinol, a copper and zinc chelating agent, can remove β amyloid plaque pathology. However, it was unclear ...
But no, in a landmark court case, the cause was shown to be a gastrointestinal drug, clioquinol, manufactured by Ciba-Geigy. ... Since then, some research has suggested that clioquinol fails to explain all the SMON cases. ...
Clioquinol (iodochlorhydroxyquin). Clobetasol Quantity limited for 30 days. proprionate Clobetasone butyrate. Clotrimazole. ...
Factor inhibiting HIF-1 alpha in complex with Clioquinol. 3kcy. Factor inhibiting HIF-1 alpha in complex with 8- ...
clioquinol / iodochlorhydroxyquin (nowadays used only as Zn chelator. ) *4-quinoline-methanols *mefloquine chlorhydrate ( ...
Aktuelle API Auditberichte • GMP-Audits der Herstelung pharmazeutischer Ausgangs- und Wirkstoffe nach ICH Q7 / EU GMP Guide Part II • Diapharm
That trial, of clioquinol (also known as PBT1) showed no statistically significant difference in cognition between active ... The authors concluded that there is no current evidence that treatment with clioquinol (PBT1) has any significant effect on ...
Treatment with an iron chelator such as clioquinol has been shown to reduce nigral iron resulting in an increase in the cell ... J. L. Billings, D. J. Hare, M. Nurjono et al., "Effects of neonatal iron feeding and chronic clioquinol administration on the ...
Treatment with Clioquinol (a metal chelator) has been shown to reduce the accumulation of Aβ species in transgenic mouse models ...
... we hypothesize that clioquinol affects them by slowing down the rate of aging," says Dr Hekimi. Exactly how clioquinol inhibits ... Clioquinol is best known as an antifungal and antiprotozoal drug; however its use as an antiporotozoal drug ended when it was ... Clioquinol has been around for 100 years and is currently used to treat athletes foot, ear infections and indigestion. [ ... This might be why clioquinol is able to work on this diversity of diseases that are all age-dependent." [McGill University ...
Clioquinol. An antifungal cream used to treat a variety of fungal infections. ...

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