A simple organophosphorus compound that inhibits DNA polymerase, especially in viruses and is used as an antiviral agent.
Organic compounds that contain phosphorus as an integral part of the molecule. Included under this heading is broad array of synthetic compounds that are used as PESTICIDES and DRUGS.
A genus of the family HERPESVIRIDAE, subfamily ALPHAHERPESVIRINAE, consisting of herpes simplex-like viruses. The type species is HERPESVIRUS 1, HUMAN.
DNA-dependent DNA polymerases found in bacteria, animal and plant cells. During the replication process, these enzymes catalyze the addition of deoxyribonucleotide residues to the end of a DNA strand in the presence of DNA as template-primer. They also possess exonuclease activity and therefore function in DNA repair.
Derivatives of ACETIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxymethane structure.
A form of herpetic keratitis characterized by the formation of small vesicles which break down and coalesce to form recurring dendritic ulcers, characteristically irregular, linear, branching, and ending in knoblike extremities. (Dictionary of Visual Science, 3d ed)
An analog of DEOXYURIDINE that inhibits viral DNA synthesis. The drug is used as an antiviral agent.
Deoxyribonucleic acid that makes up the genetic material of viruses.
An antiviral agent used in the treatment of cytomegalovirus retinitis. Foscarnet also shows activity against human herpesviruses and HIV.
An antiviral antibiotic produced by Cephalosporium aphidicola and other fungi. It inhibits the growth of eukaryotic cells and certain animal viruses by selectively inhibiting the cellular replication of DNA polymerase II or the viral-induced DNA polymerases. The drug may be useful for controlling excessive cell proliferation in patients with cancer, psoriasis or other dermatitis with little or no adverse effect upon non-multiplying cells.
A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
A group of acute infections caused by herpes simplex virus type 1 or type 2 that is characterized by the development of one or more small fluid-filled vesicles with a raised erythematous base on the skin or mucous membrane. It occurs as a primary infection or recurs due to a reactivation of a latent infection. (Dorland, 27th ed.)
Proteins found in any species of virus.
The process by which a DNA molecule is duplicated.
The type species of LYMPHOCRYPTOVIRUS, subfamily GAMMAHERPESVIRINAE, infecting B-cells in humans. It is thought to be the causative agent of INFECTIOUS MONONUCLEOSIS and is strongly associated with oral hairy leukoplakia (LEUKOPLAKIA, HAIRY;), BURKITT LYMPHOMA; and other malignancies.
Twenty-carbon compounds derived from MEVALONIC ACID or deoxyxylulose phosphate.
The functional hereditary units of VIRUSES.
A CELL LINE derived from the kidney of the African green (vervet) monkey, (CERCOPITHECUS AETHIOPS) used primarily in virus replication studies and plaque assays.
Method for measuring viral infectivity and multiplication in CULTURED CELLS. Clear lysed areas or plaques develop as the VIRAL PARTICLES are released from the infected cells during incubation. With some VIRUSES, the cells are killed by a cytopathic effect; with others, the infected cells are not killed but can be detected by their hemadsorptive ability. Sometimes the plaque cells contain VIRAL ANTIGENS which can be measured by IMMUNOFLUORESCENCE.
Established cell cultures that have the potential to propagate indefinitely.
A species of CERCOPITHECUS containing three subspecies: C. tantalus, C. pygerythrus, and C. sabeus. They are found in the forests and savannah of Africa. The African green monkey (C. pygerythrus) is the natural host of SIMIAN IMMUNODEFICIENCY VIRUS and is used in AIDS research.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
The type species of SIMPLEXVIRUS causing most forms of non-genital herpes simplex in humans. Primary infection occurs mainly in infants and young children and then the virus becomes latent in the dorsal root ganglion. It then is periodically reactivated throughout life causing mostly benign conditions.
Substances elaborated by viruses that have antigenic activity.
A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

Assessment of the allosteric mechanism of aspartate transcarbamoylase based on the crystalline structure of the unregulated catalytic subunit. (1/396)

The lack of knowledge of the three-dimensional structure of the trimeric, catalytic (C) subunit of aspartate transcarbamoylase (ATCase) has impeded understanding of the allosteric regulation of this enzyme and left unresolved the mechanism by which the active, unregulated C trimers are inactivated on incorporation into the unliganded (taut or T state) holoenzyme. Surprisingly, the isolated C trimer, based on the 1.9-A crystal structure reported here, resembles more closely the trimers in the T state enzyme than in the holoenzyme:bisubstrate-analog complex, which has been considered as the active, relaxed (R) state enzyme. Unlike the C trimer in either the T state or bisubstrate-analog-bound holoenzyme, the isolated C trimer lacks 3-fold symmetry, and the active sites are partially disordered. The flexibility of the C trimer, contrasted to the highly constrained T state ATCase, suggests that regulation of the holoenzyme involves modulating the potential for conformational changes essential for catalysis. Large differences in structure between the active C trimer and the holoenzyme:bisubstrate-analog complex call into question the view that this complex represents the activated R state of ATCase.  (+info)

Tumor, normal tissue, and plasma pharmacokinetic studies of fluorouracil biomodulation with N-phosphonacetyl-L-aspartate, folinic acid, and interferon alfa. (2/396)

PURPOSE: To evaluate the effect of N-phosphonacetyl-L-aspartate (PALA), folinic acid (FA), and interferon alfa (IFN-alpha) biomodulation on plasma fluorouracil (5FU) pharmacokinetics and tumor and liver radioactivity uptake and retention after [18F]-fluorouracil (5-[18F]-FU) administration. PATIENTS AND METHODS: Twenty-one paired pharmacokinetic studies were completed on patients with colorectal, gastric, and hepatocellular cancer, utilizing positron emission tomography (PET), which allowed the acquisition of tumor, normal tissue, and plasma pharmacokinetic data and tumor blood flow (TBF) measurements. The first PET study was completed when the patient was biomodulator-naive and was repeated on day 8 after the patient had been treated with either PALA, FA, or IFN-alpha in recognized schedules. RESULTS: TBF was an important determinant of tumor radioactivity uptake (r = .90; P < .001) and retention (r = .96; P < .001), for which radioactivity represents a composite signal of 5-[18F]-FU and [18F]-labeled metabolites and catabolites. After treatment with PALA, TBF decreased (four of four patients; P = .043), as did tumor radioactivity exposure (five of five patients; P = .0437), with no change in plasma 5FU clearance. With FA treatment, there were no differences observed in whole-body metabolism, plasma 5FU clearance, or tumor and liver pharmacokinetics. IFN-alpha had measurable effects on TBF and 5-[18F]-FU metabolism but had no apparent affect on liver blood flow. CONCLUSION: The administration of PALA and IFN-alpha produced measurable changes in plasma, tumor, and liver pharmacokinetics after 5-[18F]-FU administration. No changes were observed after FA administration. In vivo effects may negate the anticipated therapeutic advantage of 5FU biomodulation with some agents.  (+info)

Micronuclei formation with chromosome breaks and gene amplification caused by Vpr, an accessory gene of human immunodeficiency virus. (3/396)

Vpr, an accessory gene of human immunodeficiency virus, induces cell cycle abnormality by accumulating cells at the G2-M phase. We reported recently that Vpr caused both micronuclei formation and aneuploidy. Here, we show that Vpr also induced chromosome breaks and gene amplification. Expression of Vpr induced more than 10-fold increase of colonies resistant to N-(phosphonacetyl)-L-aspartate, an inhibitor of pyrimidine de novo synthesis. Fluorescence in situ hybridization analysis detected that 4 of 10 N-(phosphonacetyl)-L-aspartate resistant clones studied had intrachromosomal amplification of carbamyl-phosphate synthetase/aspartate transcarbamoylase/dihydroorotase gene. Another single clone had dicentrics. Data suggested that the Vpr-induced chromosome breaks leading to gene amplification, followed by bridge-breakage-fusion cycle, were one of the possible mechanisms of Vpr-induced genomic instability.  (+info)

The 80s loop of the catalytic chain of Escherichia coli aspartate transcarbamoylase is critical for catalysis and homotropic cooperativity. (4/396)

The X-ray structure of the Escherichia coli aspartate transcarbamoylase with the bisubstrate analog phosphonacetyl-L-aspartate (PALA) bound shows that PALA interacts with Lys84 from an adjacent catalytic chain. To probe the function of Lys84, site-specific mutagenesis was used to convert Lys84 to alanine, threonine, and asparagine. The K84N and K84T enzymes exhibited 0.08 and 0.29% of the activity of the wild-type enzyme, respectively. However, the K84A enzyme retained 12% of the activity of the wild-type enzyme. For each of these enzymes, the affinity for aspartate was reduced 5- to 10-fold, and the affinity for carbamoyl phosphate was reduced 10- to 30-fold. The enzymes K84N and K84T exhibited no appreciable cooperativity, whereas the K84A enzyme exhibited a Hill coefficient of 1.8. The residual cooperativity and enhanced activity of the K84A enzyme suggest that in this enzyme another mechanism functions to restore catalytic activity. Modeling studies as well as molecular dynamics simulations suggest that in the case of only the K84A enzyme, the lysine residue at position 83 can reorient into the active site and complement for the loss of Lys84. This hypothesis was tested by the creation and analysis of the K83A enzyme and a double mutant enzyme (DM) that has both Lys83 and Lys84 replaced by alanine. The DM enzyme has no cooperativity and exhibited 0.18% of wild-type activity, while the K83A enzyme exhibited 61% of wild-type activity. These data suggest that Lys84 is not only catalytically important, but is also essential for binding both substrates and creation of the high-activity, high-affinity active site. Since low-angle X-ray scattering demonstrated that the mutant enzymes can be converted to the R-structural state, the loss of cooperativity must be related to the inability of these mutant enzymes to form the high-activity, high-affinity active site characteristic of the R-functional state of the enzyme.  (+info)

Half of Saccharomyces cerevisiae carbamoyl phosphate synthetase produces and channels carbamoyl phosphate to the fused aspartate transcarbamoylase domain. (5/396)

The first two steps of the de novo pyrimidine biosynthetic pathway in Saccharomyces cerevisiae are catalyzed by a 240-kDa bifunctional protein encoded by the ura2 locus. Although the constituent enzymes, carbamoyl phosphate synthetase (CPSase) and aspartate transcarbamoylase (ATCase) function independently, there are interdomain interactions uniquely associated with the multifunctional protein. Both CPSase and ATCase are feedback inhibited by UTP. Moreover, the intermediate carbamoyl phosphate is channeled from the CPSase domain where it is synthesized to the ATCase domain where it is used in the synthesis of carbamoyl aspartate. To better understand these processes, a recombinant plasmid was constructed that encoded a protein lacking the amidotransferase domain and the amino half of the CPSase domain, a 100-kDa chain segment. The truncated complex consisted of the carboxyl half of the CPSase domain fused to the ATCase domain via the pDHO domain, an inactive dihydroorotase homologue that bridges the two functional domains in the native molecule. Not only was the "half CPSase" catalytically active, but it was regulated by UTP to the same extent as the parent molecule. In contrast, the ATCase domain was no longer sensitive to the nucleotide, suggesting that the two catalytic activities are controlled by distinct mechanisms. Most remarkably, isotope dilution and transient time measurements showed that the truncated complex channels carbamoyl phosphate. The overall CPSase-ATCase reaction is much less sensitive than the parent molecule to the ATCase bisubstrate analogue, N-phosphonacetyl-L-aspartate (PALA), providing evidence that the endogenously produced carbamoyl phosphate is sequestered and channeled to the ATCase active site.  (+info)

Acetylation of human hemoglobin by methyl acetylphosphate. Evidence of broad regio-selectivity revealed by NMR studies. (6/396)

The development of chemical modification agents that reduce the tendency of sickle hemoglobin (HbS) to aggregate represents an important chemotherapeutic goal. Methyl acetylphosphate (MAP) has been reported to bind to the 2,3-diphosphoglycerate (2,3-DPG) binding site of hemoglobin, where it selectively acetylates residues, resulting in increased solubility of HbS. We have prepared [1-(13)C]MAP and evaluated the adduct formation with hemoglobin using (1)H-(13)C HMQC and HSQC NMR studies. These spectra of the acetylated hemoglobin adducts showed 10-11 well resolved adduct peaks, indicating that the acetylation was not highly residue specific. The chemical shift pattern observed is in general similar to that obtained recently using [1'-(13)C]aspirin as the acetylating agent (Xu, A. S. L., Macdonald, J. M., Labotka, R. J., and London, R. E. (1999) Biochim. Biophys. Acta 1432, 333-349). Blocking the 2, 3-DPG binding site with inositol hexaphosphate (IHP) resulted in a selective reduction in intensity of adduct resonances, presumably corresponding to residues located in the 2,3-DPG binding cleft. The pattern of residue protection appeared to be identical to that observed in our previous study using IHP and labeled aspirin. Pre-acetylation of hemoglobin using unlabeled MAP, followed by acetylation with [1'-(13)C]aspirin indicated a general protective effect, with the greatest reduction of intensity for resonances corresponding to acetylated residues in the 2,3-DPG binding site. These studies indicated that both MAP and aspirin exhibit similar, although not identical, acetylation profiles and target primarily the betaLys-82 residue in the 2,3-DPG binding site, as well as sites such as betaLys-59 and alphaLys-90, which are not located in the beta-cleft of hemoglobin.  (+info)

Sequential biochemical modulation of fluorouracil with folinic acid, N-phosphonacetyl-L-aspartic acid, and interferon alfa-2a in advanced colorectal cancer. (7/396)

PURPOSE: Several agents have been evaluated for their effect as biochemical modulators of fluorouracil (5-FU) in the treatment of metastatic colorectal carcinoma. In this study, we used folinic acid (FA), N-phosphonacetyl-L-aspartic acid (PALA), and recombinant interferon alfa-2a (IFNalpha-2a) in a sequential order to assess the efficacy of this approach in patients with metastatic colorectal carcinoma. PATIENTS AND METHODS: Forty-four patients with metastatic colorectal carcinoma were enrolled onto the study. The treatment course consisted of three cycles: (cycle 1) FA 20 mg/m(2) followed by 5-FU 425 mg/m(2) on days 1 to 5; (cycle 2) PALA 250 mg/m(2) on days 29, 36, 43, and 50 and 5-FU 2,600 mg/m(2) as a 24-hour infusion on days 30, 37, 44, and 51; and (cycle 3) IFNalpha-2a 9 million units (MU) three times a week for 5 weeks beginning on day 57, with a continuous infusion of 5-FU 750 mg/m(2) on days 57 to 61, and then weekly bolus of 5-FU 750 mg/m(2)/wk on days 71, 78, and 85. Response was determined after cycle 3. RESULTS: All patients had a Zubrod performance status >/= 2, measurable disease, and had received no prior chemotherapy for their metastatic disease. A total of 212 cycles were given. Thirty-six patients were assessable for response. No complete responses were seen. Seven patients had a partial response, eight had stable disease, and 15 had progressive disease. The median duration of response was 25 weeks, and the median survival was 53 weeks. Grade 3 and 4 toxic effects included granulocytopenia, stomatitis, diarrhea, rash, nausea, and fatigue. CONCLUSION: This trial provided no evidence that sequential biochemical modulation of 5-FU in patients with metastatic colorectal carcinoma had any therapeutic advantage over conventional treatment regimens of 5-FU plus FA.  (+info)

Substitutions in the aspartate transcarbamoylase domain of hamster CAD disrupt oligomeric structure. (8/396)

Aspartate transcarbamoylase (ATCase; EC 2.1.3.2) is one of three enzymatic domains of CAD, a protein whose native structure is usually a hexamer of identical subunits. Alanine substitutions for the ATCase residues Asp-90 and Arg-269 were generated in a bicistronic vector that encodes a 6-histidine-tagged hamster CAD. Stably transfected mammalian cells expressing high levels of CAD were easily isolated and CAD purification was simplified over previous procedures. The substitutions reduce the ATCase V(max) of the altered CADs by 11-fold and 46-fold, respectively, as well as affect the enzyme's affinity for aspartate. At 25 mM Mg(2+), these substitutions cause the oligomeric CAD to dissociate into monomers. Under the same dissociating conditions, incubating the altered CAD with the ATCase substrate carbamoyl phosphate or the bisubstrate analogue N-phosphonacetyl-L-aspartate unexpectedly leads to the reformation of hexamers. Incubation with the other ATCase substrate, aspartate, has no effect. These results demonstrate that the ATCase domain is central to hexamer formation in CAD and suggest that the ATCase reaction mechanism is ordered in the same manner as the Escherichia coli ATCase. Finally, the data indicate that the binding of carbamoyl phosphate induces conformational changes that enhance the interaction of CAD subunits.  (+info)

Phosphonoacetic acid (PAA) is not a naturally occurring substance, but rather a synthetic compound that is used in medical and scientific research. It is a colorless, crystalline solid that is soluble in water.

In a medical context, PAA is an inhibitor of certain enzymes that are involved in the replication of viruses, including HIV. It works by binding to the active site of these enzymes and preventing them from carrying out their normal functions. As a result, PAA has been studied as a potential antiviral agent, although it is not currently used as a medication.

It's important to note that while PAA has shown promise in laboratory studies, its safety and efficacy have not been established in clinical trials, and it is not approved for use as a drug by regulatory agencies such as the U.S. Food and Drug Administration (FDA).

Organophosphorus compounds are a class of chemical substances that contain phosphorus bonded to organic compounds. They are used in various applications, including as plasticizers, flame retardants, pesticides (insecticides, herbicides, and nerve gases), and solvents. In medicine, they are also used in the treatment of certain conditions such as glaucoma. However, organophosphorus compounds can be toxic to humans and animals, particularly those that affect the nervous system by inhibiting acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine. Exposure to these compounds can cause symptoms such as nausea, vomiting, muscle weakness, and in severe cases, respiratory failure and death.

Simplexvirus is a genus of viruses in the family Herpesviridae, subfamily Alphaherpesvirinae. This genus contains two species: Human alphaherpesvirus 1 (also known as HSV-1 or herpes simplex virus type 1) and Human alphaherpesvirus 2 (also known as HSV-2 or herpes simplex virus type 2). These viruses are responsible for causing various medical conditions, most commonly oral and genital herpes. They are characterized by their ability to establish lifelong latency in the nervous system and reactivate periodically to cause recurrent symptoms.

DNA-directed DNA polymerase is a type of enzyme that synthesizes new strands of DNA by adding nucleotides to an existing DNA template in a 5' to 3' direction. These enzymes are essential for DNA replication, repair, and recombination. They require a single-stranded DNA template, a primer with a free 3' hydroxyl group, and the four deoxyribonucleoside triphosphates (dNTPs) as substrates to carry out the polymerization reaction.

DNA polymerases also have proofreading activity, which allows them to correct errors that occur during DNA replication by removing mismatched nucleotides and replacing them with the correct ones. This helps ensure the fidelity of the genetic information passed from one generation to the next.

There are several different types of DNA polymerases, each with specific functions and characteristics. For example, DNA polymerase I is involved in both DNA replication and repair, while DNA polymerase III is the primary enzyme responsible for DNA replication in bacteria. In eukaryotic cells, DNA polymerase alpha, beta, gamma, delta, and epsilon have distinct roles in DNA replication, repair, and maintenance.

Acetates, in a medical context, most commonly refer to compounds that contain the acetate group, which is an functional group consisting of a carbon atom bonded to two hydrogen atoms and an oxygen atom (-COO-). An example of an acetate is sodium acetate (CH3COONa), which is a salt formed from acetic acid (CH3COOH) and is often used as a buffering agent in medical solutions.

Acetates can also refer to a group of medications that contain acetate as an active ingredient, such as magnesium acetate, which is used as a laxative, or calcium acetate, which is used to treat high levels of phosphate in the blood.

In addition, acetates can also refer to a process called acetylation, which is the addition of an acetyl group (-COCH3) to a molecule. This process can be important in the metabolism and regulation of various substances within the body.

Dendritic keratitis is a specific form of keratitis, which is inflammation of the cornea. The term "dendritic" refers to the characteristic appearance of the lesion on the cornea, which resembles a branching tree or a dendrite.

Dendritic keratitis is most commonly caused by herpes simplex virus type 1 (HSV-1) infection, although other infectious and non-infectious etiologies can also produce similar lesions. The condition is characterized by the presence of a branching, dendrite-like ulcer on the corneal epithelium, often accompanied by symptoms such as eye pain, redness, photophobia (sensitivity to light), and tearing.

Treatment for dendritic keratitis typically involves antiviral medications to manage the underlying HSV-1 infection, as well as measures to promote corneal healing and reduce discomfort. It is essential to seek prompt medical attention if you suspect dendritic keratitis, as untreated or improperly managed cases can lead to serious complications, including corneal scarring, vision loss, and potential blindness.

Idoxuridine is an antiviral medication used primarily for the treatment of herpes simplex virus (HSV) infections of the eye, such as keratitis or dendritic ulcers. It works by interfering with the DNA replication of the virus, thereby inhibiting its ability to multiply and spread.

Idoxuridine is available as an ophthalmic solution (eye drops) and is typically applied directly to the affected eye every 1-2 hours while awake, for up to 2 weeks. Common side effects include local irritation, stinging, or burning upon application. Prolonged use of idoxuridine may lead to bacterial resistance or corneal toxicity, so it is important to follow your healthcare provider's instructions carefully when using this medication.

It is essential to note that idoxuridine is not commonly used today due to the development of more effective and less toxic antiviral agents for HSV infections.

Viral DNA refers to the genetic material present in viruses that consist of DNA as their core component. Deoxyribonucleic acid (DNA) is one of the two types of nucleic acids that are responsible for storing and transmitting genetic information in living organisms. Viruses are infectious agents much smaller than bacteria that can only replicate inside the cells of other organisms, called hosts.

Viral DNA can be double-stranded (dsDNA) or single-stranded (ssDNA), depending on the type of virus. Double-stranded DNA viruses have a genome made up of two complementary strands of DNA, while single-stranded DNA viruses contain only one strand of DNA.

Examples of dsDNA viruses include Adenoviruses, Herpesviruses, and Poxviruses, while ssDNA viruses include Parvoviruses and Circoviruses. Viral DNA plays a crucial role in the replication cycle of the virus, encoding for various proteins necessary for its multiplication and survival within the host cell.

Foscarnet is an antiviral medication used to treat infections caused by viruses, particularly herpes simplex virus (HSV) and varicella-zoster virus (VZV). It is a pyrophosphate analog that inhibits viral DNA polymerase, preventing the replication of viral DNA.

Foscarnet is indicated for the treatment of severe HSV infections, such as mucocutaneous HSV in immunocompromised patients, and acyclovir-resistant HSV infections. It is also used to treat VZV infections, including shingles and varicella zoster virus (VZV) infection in immunocompromised patients.

Foscarnet is administered intravenously and its use requires careful monitoring of renal function and electrolyte levels due to the potential for nephrotoxicity and electrolyte imbalances. Common side effects include nausea, vomiting, diarrhea, and headache.

Aphidicolin is an antimicrotubule agent that is specifically a inhibitor of DNA polymerase alpha. It is an antibiotic that is produced by the fungus Cephalosporium aphidicola and is used in research to study the cell cycle and DNA replication. In clinical medicine, it has been explored as a potential anticancer agent, although its use is not currently approved for this indication.

Acyclovir is an antiviral medication used for the treatment of infections caused by herpes simplex viruses (HSV) including genital herpes, cold sores, and shingles (varicella-zoster virus). It works by interfering with the replication of the virus's DNA, thereby preventing the virus from multiplying further. Acyclovir is available in various forms such as oral tablets, capsules, creams, and intravenous solutions.

The medical definition of 'Acyclovir' is:

Acyclovir (brand name Zovirax) is a synthetic nucleoside analogue that functions as an antiviral agent, specifically against herpes simplex viruses (HSV) types 1 and 2, varicella-zoster virus (VZV), and Epstein-Barr virus (EBV). Acyclovir is converted to its active form, acyclovir triphosphate, by viral thymidine kinase. This activated form then inhibits viral DNA polymerase, preventing further replication of the virus's DNA.

Acyclovir has a relatively low toxicity profile and is generally well-tolerated, although side effects such as nausea, vomiting, diarrhea, and headache can occur. In rare cases, more serious side effects such as kidney damage, seizures, or neurological problems may occur. It is important to take acyclovir exactly as directed by a healthcare provider and to report any unusual symptoms promptly.

Antiviral agents are a class of medications that are designed to treat infections caused by viruses. Unlike antibiotics, which target bacteria, antiviral agents interfere with the replication and infection mechanisms of viruses, either by inhibiting their ability to replicate or by modulating the host's immune response to the virus.

Antiviral agents are used to treat a variety of viral infections, including influenza, herpes simplex virus (HSV) infections, human immunodeficiency virus (HIV) infection, hepatitis B and C, and respiratory syncytial virus (RSV) infections.

These medications can be administered orally, intravenously, or topically, depending on the type of viral infection being treated. Some antiviral agents are also used for prophylaxis, or prevention, of certain viral infections.

It is important to note that antiviral agents are not effective against all types of viruses and may have significant side effects. Therefore, it is essential to consult with a healthcare professional before starting any antiviral therapy.

Virus replication is the process by which a virus produces copies or reproduces itself inside a host cell. This involves several steps:

1. Attachment: The virus attaches to a specific receptor on the surface of the host cell.
2. Penetration: The viral genetic material enters the host cell, either by invagination of the cell membrane or endocytosis.
3. Uncoating: The viral genetic material is released from its protective coat (capsid) inside the host cell.
4. Replication: The viral genetic material uses the host cell's machinery to produce new viral components, such as proteins and nucleic acids.
5. Assembly: The newly synthesized viral components are assembled into new virus particles.
6. Release: The newly formed viruses are released from the host cell, often through lysis (breaking) of the cell membrane or by budding off the cell membrane.

The specific mechanisms and details of virus replication can vary depending on the type of virus. Some viruses, such as DNA viruses, use the host cell's DNA polymerase to replicate their genetic material, while others, such as RNA viruses, use their own RNA-dependent RNA polymerase or reverse transcriptase enzymes. Understanding the process of virus replication is important for developing antiviral therapies and vaccines.

Microbial drug resistance is a significant medical issue that refers to the ability of microorganisms (such as bacteria, viruses, fungi, or parasites) to withstand or survive exposure to drugs or medications designed to kill them or limit their growth. This phenomenon has become a major global health concern, particularly in the context of bacterial infections, where it is also known as antibiotic resistance.

Drug resistance arises due to genetic changes in microorganisms that enable them to modify or bypass the effects of antimicrobial agents. These genetic alterations can be caused by mutations or the acquisition of resistance genes through horizontal gene transfer. The resistant microbes then replicate and multiply, forming populations that are increasingly difficult to eradicate with conventional treatments.

The consequences of drug-resistant infections include increased morbidity, mortality, healthcare costs, and the potential for widespread outbreaks. Factors contributing to the emergence and spread of microbial drug resistance include the overuse or misuse of antimicrobials, poor infection control practices, and inadequate surveillance systems.

To address this challenge, it is crucial to promote prudent antibiotic use, strengthen infection prevention and control measures, develop new antimicrobial agents, and invest in research to better understand the mechanisms underlying drug resistance.

Herpes Simplex is a viral infection caused by the Herpes Simplex Virus (HSV). There are two types of HSV: HSV-1 and HSV-2. Both types can cause sores or blisters on the skin or mucous membranes, but HSV-1 is typically associated with oral herpes (cold sores) and HSV-2 is usually linked to genital herpes. However, either type can infect any area of the body. The virus remains in the body for life and can reactivate periodically, causing recurrent outbreaks of lesions or blisters. It is transmitted through direct contact with infected skin or mucous membranes, such as during kissing or sexual activity.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

DNA replication is the biological process by which DNA makes an identical copy of itself during cell division. It is a fundamental mechanism that allows genetic information to be passed down from one generation of cells to the next. During DNA replication, each strand of the double helix serves as a template for the synthesis of a new complementary strand. This results in the creation of two identical DNA molecules. The enzymes responsible for DNA replication include helicase, which unwinds the double helix, and polymerase, which adds nucleotides to the growing strands.

Medical Definition of "Herpesvirus 4, Human" (Epstein-Barr Virus)

"Herpesvirus 4, Human," also known as Epstein-Barr virus (EBV), is a member of the Herpesviridae family and is one of the most common human viruses. It is primarily transmitted through saliva and is often referred to as the "kissing disease."

EBV is the causative agent of infectious mononucleosis (IM), also known as glandular fever, which is characterized by symptoms such as fatigue, sore throat, fever, and swollen lymph nodes. The virus can also cause other diseases, including certain types of cancer, such as Burkitt's lymphoma, Hodgkin's lymphoma, and nasopharyngeal carcinoma.

Once a person becomes infected with EBV, the virus remains in the body for the rest of their life, residing in certain white blood cells called B lymphocytes. In most people, the virus remains dormant and does not cause any further symptoms. However, in some individuals, the virus may reactivate, leading to recurrent or persistent symptoms.

EBV infection is diagnosed through various tests, including blood tests that detect antibodies against the virus or direct detection of the virus itself through polymerase chain reaction (PCR) assays. There is no cure for EBV infection, and treatment is generally supportive, focusing on relieving symptoms and managing complications. Prevention measures include practicing good hygiene, avoiding close contact with infected individuals, and not sharing personal items such as toothbrushes or drinking glasses.

Diterpenes are a class of naturally occurring compounds that are composed of four isoprene units, which is a type of hydrocarbon. They are synthesized by a wide variety of plants and animals, and are found in many different types of organisms, including fungi, insects, and marine organisms.

Diterpenes have a variety of biological activities and are used in medicine for their therapeutic effects. Some diterpenes have anti-inflammatory, antimicrobial, and antiviral properties, and are used to treat a range of conditions, including respiratory infections, skin disorders, and cancer.

Diterpenes can be further classified into different subgroups based on their chemical structure and biological activity. Some examples of diterpenes include the phytocannabinoids found in cannabis plants, such as THC and CBD, and the paclitaxel, a diterpene found in the bark of the Pacific yew tree that is used to treat cancer.

It's important to note that while some diterpenes have therapeutic potential, others may be toxic or have adverse effects, so it is essential to use them under the guidance and supervision of a healthcare professional.

Viral genes refer to the genetic material present in viruses that contains the information necessary for their replication and the production of viral proteins. In DNA viruses, the genetic material is composed of double-stranded or single-stranded DNA, while in RNA viruses, it is composed of single-stranded or double-stranded RNA.

Viral genes can be classified into three categories: early, late, and structural. Early genes encode proteins involved in the replication of the viral genome, modulation of host cell processes, and regulation of viral gene expression. Late genes encode structural proteins that make up the viral capsid or envelope. Some viruses also have structural genes that are expressed throughout their replication cycle.

Understanding the genetic makeup of viruses is crucial for developing antiviral therapies and vaccines. By targeting specific viral genes, researchers can develop drugs that inhibit viral replication and reduce the severity of viral infections. Additionally, knowledge of viral gene sequences can inform the development of vaccines that stimulate an immune response to specific viral proteins.

Vero cells are a line of cultured kidney epithelial cells that were isolated from an African green monkey (Cercopithecus aethiops) in the 1960s. They are named after the location where they were initially developed, the Vervet Research Institute in Japan.

Vero cells have the ability to divide indefinitely under certain laboratory conditions and are often used in scientific research, including virology, as a host cell for viruses to replicate. This allows researchers to study the characteristics of various viruses, such as their growth patterns and interactions with host cells. Vero cells are also used in the production of some vaccines, including those for rabies, polio, and Japanese encephalitis.

It is important to note that while Vero cells have been widely used in research and vaccine production, they can still have variations between different cell lines due to factors like passage number or culture conditions. Therefore, it's essential to specify the exact source and condition of Vero cells when reporting experimental results.

A viral plaque assay is a laboratory technique used to measure the infectivity and concentration of viruses in a sample. This method involves infecting a monolayer of cells (usually in a petri dish or multi-well plate) with a known volume of a virus-containing sample, followed by overlaying the cells with a nutrient-agar medium to restrict viral spread and enable individual plaques to form.

After an incubation period that allows for viral replication and cell death, the cells are stained, and clear areas or "plaques" become visible in the monolayer. Each plaque represents a localized region of infected and lysed cells, caused by the progeny of a single infectious virus particle. The number of plaques is then counted, and the viral titer (infectious units per milliliter or PFU/mL) is calculated based on the dilution factor and volume of the original inoculum.

Viral plaque assays are essential for determining viral titers, assessing virus-host interactions, evaluating antiviral agents, and studying viral pathogenesis.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

'Cercopithecus aethiops' is the scientific name for the monkey species more commonly known as the green monkey. It belongs to the family Cercopithecidae and is native to western Africa. The green monkey is omnivorous, with a diet that includes fruits, nuts, seeds, insects, and small vertebrates. They are known for their distinctive greenish-brown fur and long tail. Green monkeys are also important animal models in biomedical research due to their susceptibility to certain diseases, such as SIV (simian immunodeficiency virus), which is closely related to HIV.

A mutation is a permanent change in the DNA sequence of an organism's genome. Mutations can occur spontaneously or be caused by environmental factors such as exposure to radiation, chemicals, or viruses. They may have various effects on the organism, ranging from benign to harmful, depending on where they occur and whether they alter the function of essential proteins. In some cases, mutations can increase an individual's susceptibility to certain diseases or disorders, while in others, they may confer a survival advantage. Mutations are the driving force behind evolution, as they introduce new genetic variability into populations, which can then be acted upon by natural selection.

Medical Definition of "Herpesvirus 1, Human" (also known as Human Herpesvirus 1 or HHV-1):

Herpesvirus 1, Human is a type of herpesvirus that primarily causes infection in humans. It is also commonly referred to as human herpesvirus 1 (HHV-1) or oral herpes. This virus is highly contagious and can be transmitted through direct contact with infected saliva, skin, or mucous membranes.

After initial infection, the virus typically remains dormant in the body's nerve cells and may reactivate later, causing recurrent symptoms. The most common manifestation of HHV-1 infection is oral herpes, characterized by cold sores or fever blisters around the mouth and lips. In some cases, HHV-1 can also cause other conditions such as encephalitis (inflammation of the brain) and keratitis (inflammation of the eye's cornea).

There is no cure for HHV-1 infection, but antiviral medications can help manage symptoms and reduce the severity and frequency of recurrent outbreaks.

An antigen is any substance that can stimulate an immune response, particularly the production of antibodies. Viral antigens are antigens that are found on or produced by viruses. They can be proteins, glycoproteins, or carbohydrates present on the surface or inside the viral particle.

Viral antigens play a crucial role in the immune system's recognition and response to viral infections. When a virus infects a host cell, it may display its antigens on the surface of the infected cell. This allows the immune system to recognize and target the infected cells for destruction, thereby limiting the spread of the virus.

Viral antigens are also important targets for vaccines. Vaccines typically work by introducing a harmless form of a viral antigen to the body, which then stimulates the production of antibodies and memory T-cells that can recognize and respond quickly and effectively to future infections with the actual virus.

It's worth noting that different types of viruses have different antigens, and these antigens can vary between strains of the same virus. This is why there are often different vaccines available for different viral diseases, and why flu vaccines need to be updated every year to account for changes in the circulating influenza virus strains.

Cytomegalovirus (CMV) is a type of herpesvirus that can cause infection in humans. It is characterized by the enlargement of infected cells (cytomegaly) and is typically transmitted through close contact with an infected person, such as through saliva, urine, breast milk, or sexual contact.

CMV infection can also be acquired through organ transplantation, blood transfusions, or during pregnancy from mother to fetus. While many people infected with CMV experience no symptoms, it can cause serious complications in individuals with weakened immune systems, such as those undergoing cancer treatment or those who have HIV/AIDS.

In newborns, congenital CMV infection can lead to hearing loss, vision problems, and developmental delays. Pregnant women who become infected with CMV for the first time during pregnancy are at higher risk of transmitting the virus to their unborn child. There is no cure for CMV, but antiviral medications can help manage symptoms and reduce the risk of complications in severe cases.

A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

Phosphonoacetic Acid: A simple organophosphorus compound that inhibits DNA polymerase, especially in viruses and is used as an ... Carboxylic Acids: 83*Acyclic Acids*Acetic Acids: 20*Phosphonoacetic Acid: 84*Foscarnet: 738 ... Phosphonoacetic Acid (Phosphonoacetate). Subscribe to New Research on Phosphonoacetic Acid A simple organophosphorus compound ... 01/01/1982 - "Phosphonoacetic acid effective in herpesvirus infection.". 01/01/1978 - "Phosphonoacetic acid was the only ...
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Bacteriophage T4 DNA polymerase mutations that confer sensitivity to the PPi analog phosphonoacetic acid., Polymerase: T4 A737V ... Bacteriophage T4 DNA polymerase mutations that confer sensitivity to the PPi analog phosphonoacetic acid. Nucleotide ... Reference: Bacteriophage T4 DNA polymerase mutations that confer sensitivity to the PPi analog phosphonoacetic acid., ...
Li L, Murphy KM, Kanevets U, Reha-Krantz LJ (June 2005). "Sensitivity to phosphonoacetic acid: a new phenotype to probe DNA ... A longer isoform has been reported with a 26 amino acid in-frame insertion after amino acid 592 (NP_001295561.1). A pseudogene ... Lee MY, Tan CK, So AG, Downey KM (May 1980). "Purification of deoxyribonucleic acid polymerase delta from calf thymus: partial ... Motif A has 11 amino acids that are important in nucleotide incorporation and formation of the phosphodiester bond. Tyrosine ...
PPA; phosphonoacetic acid. Ribavirin; 1-0-D-ribofuranosyl-1,2,4-triazole-3-carboxamide. Ritonavir, Norvir0. Saquinavir, ... wherein X is C1-C4 alkyl), or an organic acid such as fumaric acid, acetic acid, succinic. acid. Physiologically acceptable ... acids, such as. methanesulfonic, ethanesulfonic, benzenesulfonic and p-toluenesulfonic acids; and. inorganic acids, such as ... In addition, fatty acids such as oleic acid may likewise be used in. the preparation of injectables.. The pharmaceutical ...
NDP kinase in complex with adenosine phosphonoacetic acid. 1u8w. Crystal structure of Arabidopsis thaliana nucleoside ... 2017) Nucleic Acids Res doi: 10.1093/nar/gkx922. Letunic et al. (2020) Nucleic Acids Res doi: 10.1093/nar/gkaa937 ... They provide NTPs for nucleic acid synthesis, CTP for lipid synthesis, UTP for polysaccharide synthesis and GTP for protein ... and the C-terminal part contains a high proportion of negatively charged glutamic acid residues. Thus, IC1 is a novel dynein ...
Phosphonoacetic acid ethyl ester. 86704-82-7. 3-Ethoxy thiophenol 86761-91-3. dimethyl 2-(pyrimidin-4-yl)malonate. ...
... since treatment with the DNA polymerase inhibitor phosphonoacetic acid did not induce these host-targeted effects. Taken ... since treatment with the DNA polymerase inhibitor phosphonoacetic acid did not induce these host-targeted effects. Taken ... Stiebel-Kalish H, Gaton DD, Weinberger D, Loya N, Schwartz-Ventik M et al. A comparison of the effect of hyaluronic acid versus ... Sodium hyaluronate (hyaluronic acid) promotes migration of human corneal epithelial cells in vitro. Br J Ophthalmol 2004; 88: ...
Mumbai Chemical: The Pinnacle of Phosphonoacetic Acid Distribution. From the vibrant corridors of Mumbai, rises Mumbai Chemical ...
Differential effect of phosphonoacetic acid on the expression of Epstein-Barr viral antigens and virus production ... Inhibition of Epstein-Barr virus DNA synthesis and late gene expression by phosphonoacetic acid ... A Film Detection Method for Tritium-Labelled Proteins and Nucleic Acids in Polyacrylamide Gels ...
Phosphonoacetic acid trimethyl ester,Dimethyl methoxycarbonylmethylphosphonate. Over 6000 Products In Stock and Ready to ship ...
the effects of phosphonoacetic acid on cell growth, expression of epstein-barr virus antigens, and virus production in human ... differential effect of phosphonoacetic acid on the expression of epstein-barr viral antigens and virus production.. ... growth of lymphoblastoid cells (b95-8, raji) is not inhibited by the presence of 0.4 mm phosphonoacetic acid. the synthesis of ... early viral antigens are made normally in the presence of phosphonoacetic acid, but ebv dna synthesis is blocked in cells ...
Topical 1% cyclic HPMPC and 1% phosphonoacetic acid were not quite as active as cidofovir. Ribavirin (5%) treatment reduced ... A single-amino-acid change in the GPC envelope glycoprotein of the virus is responsible for attenuation, and a single ... polyriboinosinic-polyribocytidylic acid stabilized with poly-L-lysine and carboxymethyl cellulose (poly IC:LC). Treatment with ...
Isomorphous phosphonoacetic acid salts with magnesium(II), manganese(II), cobalt(II), zinc(II) and copper(II).. Zeitschrift für ... Unexpected formation of hydroxyborazaphosphonic acid in the reaction of (N-benzyl)benzylideneimine-2-boronic acid with diethyl ... Zinc(II) complexes derived from imidazo[1,2-a]pyridin-2-ylacetic acid (HIP-2-ac):[Zn(IP-2-ac)2(H2O)] and unexpectedly, [Zn3(IP- ... Imidazo[1,2-a]pyridin-2-ylacetic acid and two pairs of isomorphous ML2(H2O)2 dihydrates (M=Ni, Co and Mn, Cd) based on its ...
Phosphonoacetic Acid [D02.705.429.875] * Tenofovir [D02.705.429.906] * Trichlorfon [D02.705.429.937] Expand All Collapse All ...
... polymerase locus of herpes simplex viruses can confer hypersensitivity to aphidicolin and resistance to phosphonoacetic acid.. ...
Bis(HexaMethylene Triamine Penta (Methylene Phosphonic Acid))BHMTPMPA is a high-efficient chelating scale inhibitor, it has ... Diethylene Triamine Penta (Methylene Phosphonic Acid) (DTPMPA). *2-Hydroxy Phosphonoacetic Acid (HPAA) ... TH-GC Green Chelating Agent (Glutamic Acid,N,N-diacetic Acid, Tetra Sodium Salt) ... Penta sodium salt of Amino Trimethylene Phosphonic Acid (ATMP•Na5). *Hepta sodium salt of Diethylene Triamine Penta (Methylene ...
The results of kinetic studies, analysis with methylation-sensitive restriction enzymes, and the use of phosphonoacetic acid, a ... The results of kinetic studies, analysis with methylation-sensitive restriction enzymes, and the use of phosphonoacetic acid, a ... Cell Line, Animals, Escherichia coli, Poxviridae, Fibroma Virus, Rabbit, Myxoma virus, Vaccinia virus, Phosphonoacetic Acid, ... DNA Restriction Enzymes, Deoxyribonucleases, Type II Site-Specific, DNA, Viral, Densitometry, Transfection, Nucleic Acid ...
67023-07-8 Phosphonic acid, (2-. ((4-. aminobutyl)amino)-. 2-. oxoethyl) Phosphonoacetic Acid/*analogs & derivatives Putrescine ... Coumaric Acids Putrescine/*analogs & derivatives. Lipids 2001 Aug;36(8):839-44 N-. (4-. azido-. 2-. nitrophenyl)putrescine 0 ... Coumaric Acids Putrescine/*analogs & derivatives Plant Extracts. Jpn J Pharmacol 1990;53(2):157 diacetylputrescine 3073-57-2 ...
2-Hydroxy Phosphonoacetic Acid (HPAA). CAS No.23783-26-8. Polyamino Polyether Methylene Phosphonic Acid(PAPEMP). ... Amino Trimethylene Phosphonic Acid (ATMP). CAS No. 6419-19-8. 1-Hydroxy Ethylidene-1,1-Diphosphonic Acid (HEDP). CAS No. 2809- ... TH-GC Green Chelating Agent (Glutamic Acid,N,N-diacetic Acid, Tetra Sodium Salt) ... Penta sodium salt of Amino Trimethylene Phosphonic Acid (ATMP•Na5). *Hepta sodium salt of Diethylene Triamine Penta (Methylene ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
D2.705.676.700 Phosphonoacetic Acid D2.241.81.38.725 D2.241.81.18.677 D2.705.639.590 D2.705.429.875 Phosphoramide Mustards ... D10.251.400.143 Butyric Acid D2.241.81.160.140 D2.241.81.114.750 D10.251.400.241.140 D10.251.400.143.500 Caffeic Acids D2.241. ... B5.80.750.450 Keto Acids D2.241.607 D2.241.755 Ketoglutaric Acids D2.241.607.465 D2.241.755.465 L-Selectin D23.50.301.264. ... Aminoethylphosphonic Acid D2.705.50 D2.705.429.249 Aminohippuric Acids D2.241.223.100.120.67 D2.241.223.100.100.100 D2.241. ...
Elliott, R.M., Bateson, A. and Kelly, D.C. (1980) Phosphonoacetic acid inhibition of frog virus 3 replication. Journal of ... Burton, R.F. (1980) The role of intracellular buffers in acid-base disturbances: mathematical modelling. Respiration Physiology ... Burton, R.F. (1980) Acid and base excretion: assessment and relationships to diet and urine composition. Comparative ...
Diethylene Triamine Penta (Methylene Phosphonic Acid) (DTPMPA). *2-Hydroxy Phosphonoacetic Acid (HPAA) ... TH-GC Green Chelating Agent (Glutamic Acid,N,N-diacetic Acid, Tetra Sodium Salt) ... Penta sodium salt of Amino Trimethylene Phosphonic Acid (ATMP•Na5). *Hepta sodium salt of Diethylene Triamine Penta (Methylene ... Tetra Sodium Salt of 1-Hydroxy Ethylidene-1,1-Diphosphonic Acid (HEDP•Na4) ...

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