Crystal deposits

Although the antibacterial spectmm is similar for many of the sulfas, chemical modifications of the parent molecule have produced compounds with a variety of absorption, metaboHsm, tissue distribution, and excretion characteristics. Administration is typically oral or by injection. When absorbed, they tend to distribute widely in the body, be metabolized by the Hver, and excreted in the urine. Toxic reactions or untoward side effects have been characterized as blood dyscrasias crystal deposition in the kidneys, especially with insufficient urinary output and allergic sensitization. Selection of organisms resistant to the sulfonamides has been observed, but has not been correlated with cross-resistance to other antibiotic families (see Antibacterial AGENTS, synthetic-sulfonamides). 

The liquid is concentrated and poured into a crystallising dish. If, on cooling, the crystals are small and massed together, the solution has been too concentrated, and must be diluted so that small, well-defined crystals deposit. A dozen or so of these are... 

The increased serum phosphorus binds to calcium in the serum, which leads to deposition of hydroxyapatite crystals throughout the body. The calcium-phosphorus (Ca-P) product reflects serum solubility. A Ca-P product greater than 75 mg2/dL2 promotes crystal deposition in the joints and eye, leading to arthritis and conjunctivitis, respectively. Soft tissue deposition primarily affects the coronary arteries of the heart, lungs, and vascular tissue and is associated with a Ca-P product greater than 55 mg2/dL2.36 The Ca-P product has been associated with increased mortality37 and is a risk factor for calcification of vascular and soft tissues.35... 

As on pure water substrates, the enantiomeric crystals of SSME did not spread on the enantiomeric SSME/palmitic acid monolayer-covered surfaces, while the spreading of the racemic crystals on the racemic film-covered water was actually enhanced. The palmitic acid crystals deposited on either racemic or enantiomeric film covered substrates spread to the same surface pressure, independent of stereochemistry. 

Fig. 4. Schematic provile of microscopic crystals deposited from vapor. The hypothetical capillary pressure is zero along the stretch aa, and is very strong at points b and c...

As found for quartz, however, such processes occurring across the Earth will necessarily sum to zero net chirality. That is, because the choice of nucleating chirality is random, the chirality of the crystals deposited from disturbed solutions is also random, and over a large number of such events, the outcomes must sum to equality. 

PolycrystalHne membrane growth proceeds by initial formation of a gel layer on the surface of the support crystallization takes place at the interface between the bulk Hquid phase and the gel layer, resulting in deposition of zeolite nuclei and crystals formed [8]. Concurrently, the crystals deposited onto the support surface continue to grow, eventually resulting in a continuous membrane layer. Postsynthesis treatment is necessary when a template is used in synthesis to activate the zeolite and open the pores. Usually this is accomplished through calcination or burn out of the organic molecule. 

Fusuyama T (1992) Intratubular crystal deposition and remineralization of carious dentin. J Biol Bucc 19, 255-262. 

Before the year 1700, chemists were unable to distinguish the differences among the various alkali metals. Sodium was often confused with potassium, which was artificially produced by slowly pouring water over wood ashes and then drying the resulting alkahne crystal deposits. Some natural alkali metals were also found at the edges of dried lakebeds and mines and... 

Gout increased uric acid resulting in sodium urate crystals deposited in the joints... 

Pharmacoiogy The exact mechanism of action of colchicine in gout is not known. Colchicine apparently exerts its effect by reducing the inflammatory response to the deposited crystals and also by diminishing phagocytosis. Colchicine diminishes lactic acid production by leukocytes directly and by diminishing phagocytosis and thereby interrupts the cycle of urate crystal deposition and inflammatory response that sustains the acute attack. 

Clinical manifestations occur in three phases. In the neurological stage, the patient appears intoxicated, with slurred speech, ataxia, stupor, and hallucinations, and may be comatose, with respiratory depression. The cardiopulmonary stage is delayed by 12-24 hours, when hypotension, tachycardia, muscle tenderness and congestive cardiac failure are seen. After 1-3 days the renal stage supervenes, with loin pain, crystalluria, oliguria and renal failure, as a result of calcium oxalate crystal deposition in the renal tract. Sequestration of calcium can cause profound hypocalcaemia, tetany, and cardiac arrhythmia. 

Rheumatic disease is defined as disease of connective tissue and medical disorders of the musculoskeletal system . The medical discipline concerned with these diseases is referred to as rheumatology. The majority of rheumatic diseases are soft tissue rheumatism and nonspecific low back pain (LBP), autoimmune inflammatory rheumatic diseases, osteoarthritis (OA), osteoporosis, crystal-deposition disease and infectious arthritis. 

The etiologies of the autoimmune inflammatory diseases, OA, osteoporosis and crystal-deposition disease are still not known in exact details. This is in contrast with impressive molecular insights gained recently. However, there is consensus that manifestations of autoimmune diseases are precipitated by either acute and/or chronic interactions of genetic and environmental risk factors. 

Arthropathies associated with crystals deposition are acute gouty arthritis, chronic gout and chronic tophaceous gout due to monosodium urate crystals. Then there is acute pseudogout and chronic pyrophosphate arthropathy caused by calcium pyrophosphate dehydrate crystals. Acute calcific periarthritis, acute hydroxylapatite arthritis and chronic hydroxyapatite arthritis including Milwaukee-shoulder-knee syndrome are due to basic calcium-phosphate-hydroxyapatite crystals. 

Gouty arthritis is an inflammatory response to the deposition of monosodium urate monohydrate crystals secondary to hyperuricemia. It is called monosodium urate crystal deposition disease. Hyperuricemia is a serum urate concentration > 7 mg% in males and >6 mg% in females. Hyperuricemia results from overproduction (10-15% of individuals) or a renal excretion of urate lower than 400 mg uric acid/24 hours (85-90% of individuals). The urate under-excretors have a urate clearance of <6 ml/min or a urate to creatinine clearance ratio of <6%. The combination of a relative excess of dietary purine consumption together with urate under-excretion is often the basis for hyperuricemia. 

Pharmaceutical therapy of acute arthritis of crystal-deposition disease is effective, in particular for gout and hyperuricemia. Treatment is directed towards termination of acute arthritis, prevention of recurring attacks and prophylaxis and reversal of complications of chronic gout. Such complications include tophi, urolithiasis, nephropathy and with hyperuricemia associated medical problems that can be prevented, inhibited, and sometimes reversed. 

Mechanism of Action An alkaloid that decreases leukocyte motility, phagocytosis, and lactic acid production. Therapeutic Effect Decreases urate crystal deposits and reduces inflammatory process. 

Nephrotoxicity Pre-renal failure, e.g. hypotension following 3 lactam-induced anaphylaxis Obstructive nephropathy, e.g. crystal deposition following cephalosixrin administration... 

Gout is a metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate in joints and cartilage. Uric acid renal calculi, tophi, and interstitial nephritis may also occur. Gout is usually associated with hyperuricemia, high serum levels of uric acid, a poorly soluble substance that is the major end product of purine metabolism. In most mammals, uricase converts uric acid to the more soluble allantoin this enzyme is absent in humans. While clinical gouty episodes are associated with hyperuricemia, most individuals with hyperuricemia may never develop a clinical event from urate crystal deposition. 

Transfer the phosphonium iodide crystals deposited on the adapter walls into the receiver by carefully heating the adapter with a weak burner flame. Seal the Wurtz test tube (wear eye protection ). Weigh the ampoule and the remaining part of the test tube. Calculate the yield in per cent. Write the equations of the reactions. 

In crystallizing salts from solution, it frequently happens that it is possible to obtain more than one hydrate. In all such cases, a perfectly definite temperature can be found above which the one hydrate will deposit, and below which the other one with a larger number of molecules of water of hydration appears. Thus, above 38°, zinc sulfate deposits crystals of the composition ZnS04 6H20, while crystals deposited below that temperature have the formula ZnS04-7H20. This is also called a transition point. 

Composition. Crystals deposited from ethanol solution as well-formed thin plates. The fatty acid content of the crystals is given in Table I. For all chain lengths the acid content approximates closely that required for 1 to 1 stoichiometry. This is also the case for most of the acid-soaps prepared by the petroleum ether route the low values of titratable acid in some instances are ascribable to the presence of free soap. 

To a solution of 16.3 g 2,5-dimethoxy-3,4-dimethylbenzaldehyde in 50 mL nitromethane there was added 3.0 g anhydrous ammonium acetate, and the mixture was heated on the steam bath overnight. There was then added an equal volume of MeOH, and with cooling there was obtained a fine crop of yellow crystals. These were removed by filtration, washed with MeOH, and air dried to provide 4.4 g of 2,5-dimethoxy-3,4-dimethy 1-6-nitrostyrene with a mp of 120-121 °C which was not improved by recrystallization from MeOH (50 mL/g). The mother liquors of the above filtration were diluted with H20 to the point of per-manent turbidity, then set aside in a cold box. There wasachunky, granular, tomato-red crystal deposited which weighed 2.5 g when dry. It had a mp of 118-119.5 °C, which was undepressed in mixed mp with the yellow sample. Both forms had identical NMR spectra (2.20, 2.25 CH, 3.72, 3.84 OCH, 6.80 ArH 7.76, 8.28 CH=CH, with 14 cycle splitting), infrared spectra, ultra violet spectra (max. 324 nm with shoulder at 366 nm in EtOH, two peaks at 309 and 355 nm in hexane), and microanalyses. Anal. (C HlsN04) C,H,N. 

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