Hydrazones
Phosgene
Ochrobactrum anthropi
Isatin
Hydrazines
Imines
Cyclization
Ketones
Phenylhydrazines
Molecular Structure
Stereoisomerism
Role of interleukin (IL)-2 receptor beta-chain subdomains and Shc in p38 mitogen-activated protein (MAP) kinase and p54 MAP kinase (stress-activated protein Kinase/c-Jun N-terminal kinase) activation. IL-2-driven proliferation is independent of p38 and p54 MAP kinase activation. (1/545)
We have shown recently that interleukin (IL)-2 activates the mitogen-activated protein (MAP) kinase family members p38 (HOG1/stress-activated protein kinase II) and p54 (c-Jun N-terminal kinase/stress-activated protein kinase I). Furthermore, the p38 MAP kinase inhibitor SB203580 inhibited IL-2-driven T cell proliferation, suggesting that p38 MAP kinase might be involved in mediating proliferative signals. In this study, using transfected BA/F3 cell lines, it is shown that both the acidic domain and the membrane-proximal serine-rich region of the IL-2Rbeta chain are required for p38 and p54 MAP kinase activation and that, as for p42/44 MAP kinase, this activation requires the Tyr338 residue of the acidic domain, the binding site for Shc. It is well established that the acidic domain of the IL-2Rbeta chain is dispensable for IL-2-driven proliferation, and thus our observations suggest that neither p38 nor p54 MAP kinase activation is required for IL-2-driven proliferation of BA/F3 cells. In addition, the tetravalent guanylhydrazone inhibitor of proinflammatory cytokine production, CNI-1493, can block the activation of p54 and p38 MAP kinases by IL-2 but has no effect on IL-2-driven proliferation of BA/F3 cells, activated primary T cells, or a cytotoxic T cell line. Furthermore, our observations provide evidence for the existence of an additional, unknown target of the p38 MAP kinase inhibitor SB203580, the activation of which is essential for mitogenic signaling by IL-2. (+info)Renal ischemia/reperfusion leads to macrophage-mediated increase in pulmonary vascular permeability. (2/545)
BACKGROUND: Despite the advent of dialysis, survival with acute renal failure when associated with multiorgan failure is poor. The development of lung injury after shock or visceral ischemia has been shown; however, the effects of isolated renal ischemia/reperfusion injury (IRI) on the lungs are unclear. We hypothesized that isolated renal IRI could alter pulmonary vascular permeability (PVP) and that macrophages could be important mediators in this response. METHODS: Rats (N = 5 per group) underwent renal ischemia for 30 minutes, followed by reperfusion. Lung vascular permeability was evaluated by quantitation of Evans blue dye extravasation from vascular space to lung parenchyma at 1, 24, 48, or 96 hours after reperfusion. Serum was collected for blood urea nitrogen and creatinine at each time point. To examine the role of the macrophage, the macrophage pacifant CNI-1493, which inhibits the release of macrophage-derived inflammatory products, was administered in a blinded fashion during renal IRI. RESULTS: PVP was significantly (P < 0.05) increased at 24 hours and peaked at 48 hours after IRI compared with shams as well as baseline levels. PVP after IRI became similar to shams after 96 hours. This correlated with increases in blood urea nitrogen and creatinine at similar time points. At 48 hours, CNI-1493 significantly abrogated the increase in PVP compared with IRI alone. However, CNI-1493 did not alter the course of the acute renal failure. Pulmonary histology demonstrated interstitial edema, alveolar hemorrhage, and red blood cell sludging after renal IRI, which was partially attenuated by CNI-1493. CONCLUSIONS: Increased PVP develops after isolated renal IRI, and macrophage-derived products are mediators in this response. These findings have implications for understanding the mechanisms underlying respiratory dysfunction associated with acute renal failure. (+info)Levosimendan: effects of a calcium sensitizer on function and arrhythmias and cyclic nucleotide levels during ischemia/reperfusion in the Langendorff-perfused guinea pig heart. (3/545)
The majority of clinically used inotropes act by increasing cytosolic calcium levels, which may hypothetically worsen reperfusion stunning and provoke arrhythmias. We tested the hypothesis that the calcium sensitizer levosimendan (levo) given during ischemia alone or ischemia and reperfusion would improve reperfusion function without promoting arrhythmias. The Langendorff-perfused guinea pig heart, subjected to 40-min low-flow ischemia (0.4 ml/min) with or without levo (10-300 nM) given during ischemia or ischemia/reperfusion was used. Left ventricular developed pressure (LVDP) was used as an index of mechanical function. The effect of levo (300 nM) or dobutamine (0.1 microM) on the incidence of ischemia/reperfusion arrhythmias was also investigated. Control hearts (vehicle-perfused) had LVDPs of 69.4 +/- 2.1 mm Hg whereas hearts treated with levo during ischemia and reperfusion (300 nM) had LVDPs of 104.5 +/- 2.7 mm Hg (p <.05). Hearts treated with levo during ischemia alone (10 nM) had reperfusion LVDPs of 95.8 +/- 4.2 mm Hg (p <.05) after 30-min reperfusion. Hearts treated with both levo and 10 microM glibenclamide (K(ATP) channel blocker) during ischemia had reperfusion LVDPs of 73.4 +/- 4.3 mm Hg after 30-min reperfusion. Of control hearts, 25% developed reperfusion ventricular tachycardia but not ventricular fibrillation. Levo-treated hearts had no ischemia/reperfusion arrhythmias whereas 83% (p <.05 versus control) of dobutamine-treated hearts developed ventricular tachycardia and 33% (p <.05 versus levo) developed reperfusion ventricular fibrillation. Levo improved reperfusion function without promoting arrhythmias in this model. This was possibly achieved by opening the K(ATP) channels during ischemia and sensitizing myocardial contractile apparatus instead of elevating cytosolic calcium levels in reperfused hearts. (+info)Drug binding to cardiac troponin C. (4/545)
Compounds that sensitize cardiac muscle to Ca(2+) by intervening at the level of regulatory thin filament proteins would have potential therapeutic benefit in the treatment of myocardial infarctions. Two putative Ca(2+) sensitizers, EMD 57033 and levosimendan, are reported to bind to cardiac troponin C (cTnC). In this study, we use heteronuclear NMR techniques to study drug binding to [methyl-(13)C]methionine-labeled cTnC when free or when complexed with cardiac troponin I (cTnI). In the absence of Ca(2+), neither drug interacted with cTnC. In the presence of Ca(2+), one molecule of EMD 57033 bound specifically to the C-terminal domain of free cTnC. NMR and equilibrium dialysis failed to demonstrate binding of levosimendan to free cTnC, and the presence of levosimendan had no apparent effect on the Ca(2+) binding affinity of cTnC. Changes in the N-terminal methionine methyl chemical shifts in cTnC upon association with cTnI suggest that cTnI associates with the A-B helical interface and the N terminus of the central helix in cTnC. NMR experiments failed to show evidence of binding of levosimendan to the cTnC.cTnI complex. However, levosimendan covalently bound to a small percentage of free cTnC after prolonged incubation with the protein. These findings suggest that levosimendan exerts its positive inotropic effect by mechanisms that do not involve binding to cTnC. (+info)Diabetes induces an impairment in the proteolytic activity against oxidized proteins and a heterogeneous effect in nonenzymatic protein modifications in the cytosol of rat liver and kidney. (5/545)
It is assumed that increased oxidative stress contributes to the development of complications in diabetes. In this study, several markers of protein structural modifications directly induced by free radicals were investigated in the liver and kidney cytosolic fractions of rats with streptozotocin-induced diabetes. Sulfydryl residue and side-chain amino group analyses, as well as immunoblotting and chromatographic measurements of protein-bound carbonyl, suggest that protein oxidative modification is not increased by diabetes, with the exception of sulfydryl groups in renal cytosol. The levels of the glycation-derived carbonyl N epsilon-fructosyl-lysine are significantly increased by diabetes. Furthermore, unchanged proteolytic activity against in vivo-oxidized proteins, significant decreases both in activity against H2O2-modified proteins and in proteasome activity, measured by the degradation of a specific fluorogenic substrate, suggest that the unchanged oxidative protein modification in the diabetic state cannot be attributed to an increased cytosolic proteolytic activity in these tissues. These results provide evidence against a generalized increase in protein oxidative damage and demonstrate a diabetes-induced alteration in cytosolic proteolytic pathways, suggesting that proteasome activity may be impaired in these organs. (+info)W-7 induces [Ca(2+)](i) increases in Madin-Darby canine kidney (MDCK) cells. (6/545)
The effect of W-7 [N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride] on Ca(2+) signaling in Madin-Darby canine kidney cells was investigated. W-7 (0.1-1 mM) induced a [Ca(2+)](i) increase, which comprised an initial increase and a plateau. Ca(2+) removal inhibited the Ca(2+) signals by 80%, suggesting that W-7 activated external Ca(2+) influx and internal Ca(2+) release. Pretreatment with the mitochondrial uncoupler carbonylcyanide m-chlorophenylhydrazone (2 microM) and the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (1 microM) abolished the internal Ca(2+) release induced by 0.5 mM W-7; conversely, pretreatment with W-7 prevented thapsigargin and carbonylcyanide m-chlorophenylhydrazone from releasing internal Ca(2+). W-7 (0.2 mM) induced Mn(2+) quench of fura-2 fluorescence, which was inhibited by La(3+) (0.1 mM) by 80%. La(3+) (0.1 mM) partly inhibited 0.2 mM W-7-induced [Ca(2+)](i) increase. Addition of 5 mM Ca(2+) induced a significant [Ca(2+)](i) increase after pretreating with 0.2 to 1 mM W-7 in Ca(2+)-free medium for 5 min, suggesting that W-7 induced capacitative Ca(2+) entry. W-7 (0.5 mM) potentiated the capacitative Ca(2+) entry induced by 1 microM thapsigargin by 15%. Pretreatment with aristolochic acid (40 microM) to inhibit phospholipase A(2) reduced 0.5 mM W-7-induced internal Ca(2+) release and external Ca(2+) influx by 25 and 80%, respectively. Inhibition of phospholipase C with U73122 (2 microM) or inhibition of phospholipase D with propranolol (0.1 mM) had no effect on the internal Ca(2+) release induced by 0.5 mM W-7. It remains unclear whether W-7 induced [Ca(2+)](i) increases via inhibition of calmodulin. Three other calmodulin inhibitors (phenoxybenzamine, trifluoperazine, and fluphenazine-N-chloroethane) did not alter resting [Ca(2+)](i). (+info)Direct measurement of aluminum uptake and distribution in single cells of Chara corallina. (7/545)
Quantitative information on the uptake and distribution of Al at the cellular level is required to understand mechanisms of Al toxicity, but direct measurement of uptake across the plasma membrane has remained elusive. We measured rates of Al transport across membranes in single cells of Chara corallina using the rare (26)Al isotope, an emerging technology (accelerator mass spectrometry), and a surgical technique for isolating subcellular compartments. Accumulation of Al in the cell wall dominated total uptake (71-318 microgram m(-2) min(-1)), although transport across the plasma membrane was detectable (71-540 ng m(-2) min(-1)) within 30 min of exposure. Transport across the tonoplast was initially negligible, but accelerated to rates approximating uptake across the plasma membrane. The avacuolate protoplasm showed signs of saturation after 60 min, but continued movement across the plasma membrane was supported by sequestration in the vacuole. Saturation of all compartments was observed after 12 to 24 h. Accumulation of Al in the cell wall reflected variation in [Al(3+)] induced by changes in Al supply or complexing ligands, but was unaffected by pH. In contrast, transport across the plasma membrane peaked at pH 4.3 and increased when [Al(3+)] was reduced by complexing ligands. Cold temperature (4 degrees C) reduced accumulation in the cell wall and protoplasm, whereas 2,4-dinitrophenol and m-chlorocarbonylcyanidephenyl hydrazone increased membrane transport by 12- to 13-fold. Our data suggest that the cell wall is the major site of Al accumulation. Nonetheless, membrane transport occurs within minutes of exposure and is supported by subsequent sequestration in the vacuole. The rapid delivery of Al to the protoplasm suggests that intracellular lesions may be possible. (+info)Selection for high immunogenicity in drug-resistant sublines of murine lymphomas demonstrated by plaque assay. (8/545)
The immunogenicity of lymphoma L1210 and three L1210 sublines, resistant to methylglyoxal bis(guanylhydrazone), 4,4'-diacetyldiphenylurea bis(guanylhydrazone), or guanazole (L1210/GZL), respectively, was evaluated. Syngeneic DBA/2J mice were given a single i.p. injection of serially diluted suspension of irradiated cells from L1210 or L1210 sublines. Five days later spleen cells from the immunized mice were tested for the presence of plaque-forming cells using the immunizing lymphoma cell lines as target. Sera collected from the animals were examined for cytolytic antibody activity by lysis in gel using the same target cells. For comparison, the H-2 immunogenicity of L1210 and its sublines was investigated in H-2-incompatible allogeneic mice. The following results were obtained. (a) All the sublines showed increased immunogenicity and susceptibility to lysis as compared to L1210 cells. The number of plaque-forming cells/spleen ranged from 100 for L1210 to 4450 for L1210/GZL, the most immunogenic subline, and the antibody titer ranged from 1/8 for L1210 to 1/128 for L1210/GZL. (b) All the sublines carried common tumor-associated antigens that apparently made primary contributions to the increased immunogenicity. (c) The common tumor-associated antigens were also expressed on L1210 cells, although in a lesser defree, as evidenced by the definite, albeit low, capacity of L1210 cells to absorb DBA/2J anti-L1210/GZL antibodies. (d) Spleen and thymus cells of DBA/2J mice as well as unrelated murine ascites tumor cells did not cause significant absorption of these antibodies. (e) Only a partial inverse relationship could be demonstrated between tumor-associated antigens but the lowest for H-2. The above results would seem compatible with the hypothesis that the increased immunogenicity of drug-resistant L1210 sublines is attributable to the selection of preexisting highly immunogenic cells during immunosuppression by treatments selecting for drug resistance. (+info)A hydrazone is not a medical term per se, but rather a chemical compound. However, it's important for medical professionals to understand the properties and reactions of various chemical compounds, including hydrazones, in the context of pharmacology, toxicology, and medicinal chemistry. Here's a general definition:
Hydrazones are organic compounds that contain a functional group with the structure R1R2C=NNR3, where R1, R2, and R3 are hydrogen atoms or organic groups. They are formed by the condensation reaction of a carbonyl compound (aldehyde or ketone) with hydrazine or its derivatives. Hydrazones can exhibit various biological activities, such as antibacterial, antifungal, and anticancer properties. Some hydrazones are also used as intermediates in the synthesis of pharmaceuticals and other organic compounds.
Phosgene is not a medical condition, but it is an important chemical compound with significant medical implications. Medically, phosgene is most relevant as a potent chemical warfare agent and a severe pulmonary irritant. Here's the medical definition of phosgene:
Phosgene (COCl2): A highly toxic and reactive gas at room temperature with a characteristic odor reminiscent of freshly cut hay or grass. It is denser than air, allowing it to accumulate in low-lying areas. Exposure to phosgene primarily affects the respiratory system, causing symptoms ranging from mild irritation to severe pulmonary edema and potentially fatal respiratory failure.
Inhaling high concentrations of phosgene can lead to immediate choking sensations, coughing, chest pain, and difficulty breathing. Delayed symptoms may include fever, cyanosis (bluish discoloration of the skin due to insufficient oxygen), and pulmonary edema (fluid accumulation in the lungs). The onset of these severe symptoms can be rapid or take up to 48 hours after exposure.
Medical management of phosgene exposure primarily focuses on supportive care, including administering supplemental oxygen, bronchodilators, and corticosteroids to reduce inflammation. In severe cases, mechanical ventilation may be necessary to maintain adequate gas exchange in the lungs.
"Ochrobactrum anthropi" is a gram-negative, rod-shaped bacterium that is found in various environments, including soil, water, and clinical samples. It is a conditional pathogen, meaning it can cause infection under certain circumstances, particularly in immunocompromised individuals. Infections caused by Ochrobactrum anthropi are often associated with medical devices or procedures, such as catheter-related bacteremia, pneumonia, and wound infections. It is inherently resistant to many antibiotics, which can make treatment challenging.
Isatin is not a medical term, but rather an organic compound that has been used in various biochemical and medicinal research contexts. Here's the chemical definition:
Isatin, also known as indole-2,3-dione, is an organic compound with the formula C8H5NO2. It is a derivative of indole and consists of a benzene ring fused to a pyrrole ring, with two ketone functional groups (=O) at positions 2 and 3. Isatin is a white crystalline solid that is slightly soluble in water and more soluble in organic solvents. It occurs naturally in some plants and animals and can be synthesized in the laboratory.
In medical and biochemical research, isatin has been studied for its potential role as an inhibitor of various enzymes and biological targets, including monoamine oxidases, tyrosinase, and carbonic anhydrase. Some isatin derivatives have shown promising results in preclinical studies for the treatment of various diseases, such as cancer, neurodegenerative disorders, and infectious diseases. However, more research is needed to determine their safety and efficacy in humans before they can be approved for medical use.
Fluorine compounds are chemical substances that contain fluorine, the most electronegative and reactive of all elements, as an integral part of their molecular structure. Fluorine is a member of the halogen group in the periodic table and readily forms compounds with many other elements.
Fluoride is the most common form of fluorine compound found in nature, existing as an ion (F-) in minerals such as fluorspar (calcium fluoride, CaF2) and cryolite (sodium aluminum fluoride, Na3AlF6). Fluoride ions can replace hydroxyl ions (OH-) in the crystal structure of tooth enamel, making it more resistant to acid attack by bacteria, which is why fluoride is often added to drinking water and dental products.
Other examples of fluorine compounds include chlorofluorocarbons (CFCs), hydrofluoric acid (HF), sulfur hexafluoride (SF6), and uranium hexafluoride (UF6). Fluorine compounds have a wide range of applications, including use as refrigerants, solvents, pharmaceuticals, and materials for the semiconductor industry. However, some fluorine compounds can be highly toxic or reactive, so they must be handled with care.
Hydrazines are not a medical term, but rather a class of organic compounds containing the functional group N-NH2. They are used in various industrial and chemical applications, including the production of polymers, pharmaceuticals, and agrochemicals. However, some hydrazines have been studied for their potential therapeutic uses, such as in the treatment of cancer and cardiovascular diseases. Exposure to high levels of hydrazines can be toxic and may cause damage to the liver, kidneys, and central nervous system. Therefore, medical professionals should be aware of the potential health hazards associated with hydrazine exposure.
In the field of organic chemistry, imines are a class of compounds that contain a functional group with the general structure =CR-NR', where C=R and R' can be either alkyl or aryl groups. Imines are also commonly referred to as Schiff bases. They are formed by the condensation of an aldehyde or ketone with a primary amine, resulting in the loss of a molecule of water.
It is important to note that imines do not have a direct medical application, but they can be used as intermediates in the synthesis of various pharmaceuticals and bioactive compounds. Additionally, some imines have been found to exhibit biological activity, such as antimicrobial or anticancer properties. However, these are areas of ongoing research and development.
Cyclization is a chemical process that involves forming a cyclic structure or ring-shaped molecule from a linear or open-chain compound. In the context of medicinal chemistry and drug design, cyclization reactions are often used to synthesize complex molecules, including drugs, by creating rings or fused ring systems within the molecule's structure.
Cyclization can occur through various mechanisms, such as intramolecular nucleophilic substitution, electrophilic addition, or radical reactions. The resulting cyclized compounds may exhibit different chemical and biological properties compared to their linear precursors, making them valuable targets for drug discovery and development.
In some cases, the cyclization process can lead to the formation of stereocenters within the molecule, which can impact its three-dimensional shape and how it interacts with biological targets. Therefore, controlling the stereochemistry during cyclization reactions is crucial in medicinal chemistry to optimize the desired biological activity.
Overall, cyclization plays a significant role in the design and synthesis of many pharmaceutical compounds, enabling the creation of complex structures that can interact specifically with biological targets for therapeutic purposes.
Ketones are organic compounds that contain a carbon atom bound to two oxygen atoms and a central carbon atom bonded to two additional carbon groups through single bonds. In the context of human physiology, ketones are primarily produced as byproducts when the body breaks down fat for energy in a process called ketosis.
Specifically, under conditions of low carbohydrate availability or prolonged fasting, the liver converts fatty acids into ketone bodies, which can then be used as an alternative fuel source for the brain and other organs. The three main types of ketones produced in the human body are acetoacetate, beta-hydroxybutyrate, and acetone.
Elevated levels of ketones in the blood, known as ketonemia, can occur in various medical conditions such as diabetes, starvation, alcoholism, and high-fat/low-carbohydrate diets. While moderate levels of ketosis are generally considered safe, severe ketosis can lead to a life-threatening condition called diabetic ketoacidosis (DKA) in people with diabetes.
Phenylhydrazines are organic compounds that contain a phenyl group (a benzene ring with a hydrogen atom substituted by a hydroxy group) and a hydrazine group (-NH-NH2). They are aromatic amines that have been used in various chemical reactions, including the formation of azos and hydrazones. In medicine, phenylhydrazines were once used as vasodilators to treat angina pectoris, but their use has largely been discontinued due to their toxicity and potential carcinogenicity.
Aldehydes are a class of organic compounds characterized by the presence of a functional group consisting of a carbon atom bonded to a hydrogen atom and a double bonded oxygen atom, also known as a formyl or aldehyde group. The general chemical structure of an aldehyde is R-CHO, where R represents a hydrocarbon chain.
Aldehydes are important in biochemistry and medicine as they are involved in various metabolic processes and are found in many biological molecules. For example, glucose is converted to pyruvate through a series of reactions that involve aldehyde intermediates. Additionally, some aldehydes have been identified as toxicants or environmental pollutants, such as formaldehyde, which is a known carcinogen and respiratory irritant.
Formaldehyde is also commonly used in medical and laboratory settings for its disinfectant properties and as a fixative for tissue samples. However, exposure to high levels of formaldehyde can be harmful to human health, causing symptoms such as coughing, wheezing, and irritation of the eyes, nose, and throat. Therefore, appropriate safety measures must be taken when handling aldehydes in medical and laboratory settings.
Molecular structure, in the context of biochemistry and molecular biology, refers to the arrangement and organization of atoms and chemical bonds within a molecule. It describes the three-dimensional layout of the constituent elements, including their spatial relationships, bond lengths, and angles. Understanding molecular structure is crucial for elucidating the functions and reactivities of biological macromolecules such as proteins, nucleic acids, lipids, and carbohydrates. Various experimental techniques, like X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and cryo-electron microscopy (cryo-EM), are employed to determine molecular structures at atomic resolution, providing valuable insights into their biological roles and potential therapeutic targets.
Stereoisomerism is a type of isomerism (structural arrangement of atoms) in which molecules have the same molecular formula and sequence of bonded atoms, but differ in the three-dimensional orientation of their atoms in space. This occurs when the molecule contains asymmetric carbon atoms or other rigid structures that prevent free rotation, leading to distinct spatial arrangements of groups of atoms around a central point. Stereoisomers can have different chemical and physical properties, such as optical activity, boiling points, and reactivities, due to differences in their shape and the way they interact with other molecules.
There are two main types of stereoisomerism: enantiomers (mirror-image isomers) and diastereomers (non-mirror-image isomers). Enantiomers are pairs of stereoisomers that are mirror images of each other, but cannot be superimposed on one another. Diastereomers, on the other hand, are non-mirror-image stereoisomers that have different physical and chemical properties.
Stereoisomerism is an important concept in chemistry and biology, as it can affect the biological activity of molecules, such as drugs and natural products. For example, some enantiomers of a drug may be active, while others are inactive or even toxic. Therefore, understanding stereoisomerism is crucial for designing and synthesizing effective and safe drugs.
Magnetic Resonance Spectroscopy (MRS) is a non-invasive diagnostic technique that provides information about the biochemical composition of tissues, including their metabolic state. It is often used in conjunction with Magnetic Resonance Imaging (MRI) to analyze various metabolites within body tissues, such as the brain, heart, liver, and muscles.
During MRS, a strong magnetic field, radio waves, and a computer are used to produce detailed images and data about the concentration of specific metabolites in the targeted tissue or organ. This technique can help detect abnormalities related to energy metabolism, neurotransmitter levels, pH balance, and other biochemical processes, which can be useful for diagnosing and monitoring various medical conditions, including cancer, neurological disorders, and metabolic diseases.
There are different types of MRS, such as Proton (^1^H) MRS, Phosphorus-31 (^31^P) MRS, and Carbon-13 (^13^C) MRS, each focusing on specific elements or metabolites within the body. The choice of MRS technique depends on the clinical question being addressed and the type of information needed for diagnosis or monitoring purposes.
Hydrazone - Wikipedia
Acetone, 2,4,6-trichlorophenyl hydrazone
Guinot Hydrazone - All Skin Types | FragranceNet.com®
Benzaldehyde, 4-(octadecyloxy)-, (4-nitrophenyl)hydrazone,Benzaldehyde, 4-(octadecylthio)- Suppliers & Manufacturers
Hydrazone-based boron difluoride complexes as triplet photosensitizers for singlet oxygen generation - Chemical Communications ...
Zinc(II)-Sterol Hydrazone Complex as a Potent Anti- Leishmania Agent: Synthesis, Characterization, and Insight into Its...
Carboligation of 5-(hydroxymethyl)furfural via whole-cell catalysis to form C12 furan derivatives and their use for hydrazone...
Analgesic and anti-inflammatory activities of salicylaldehyde 2-chlorobenzoyl hydrazone (H2LASSBio-466), salicylaldehyde 4...
Dicopper(II) Complexes of the Antitumor Analogues Acylbis(salicylaldehyde hydrazones) and Crystal Structures of Monomeric [Cu2...
Guinot Hydrazone Peaux
Douche Soin Hydrazone - Guinot
Comparison of Ullmann/RCM and Ullmann/bis-hydrazone coupling reactions; New access to benzodithiophenes for dye-sensitized...
Hydrazone Moisturizing Shower Cream | Shifeon Health & Beauty
Guinot: Hydrazone Corps Body Lotion | Elmwood Shop
3,5 Diamino Benzoic Acid - 4 Sulpho Hydrazone Manufacturer
4 Sulpho Hydrazone Manufacturers, Suppliers, Exporters, Importers in India
3-Methyl-2-Benzothiazolinone Hydrazone HCL AR (MBTH) - Labort
Hydrazone Shower Care - 200ml - Luxe Beauty and Wellness Spa
GUINOT Hydrazone drėkinamasis kremas (visų tipų odai), 50 ml - Sugihara PRO
Guinot Hydrazone All Skin Type 50ml - Roots Hair and Beauty Salon Qatar
Correlating Structure and KA2 Catalytic Activity of Zn(II) Hydrazone Complexes | GDCh.app