Avian development

Drake VJ, Koprowski SL, Hu N, et al. Cardiogenic effects of trichloroethylene and trichloroacetic acid following exposure during heart specification of avian development. Toxicol Sci 2006 94(1) 153 62. 

Fainsod, A. Gruenbaum, Y. (1994). Homeobox genes in avian development. Poult. Sci. Rev., 6, in press. 

Knapp, LW., Shames, R.B., Barnes, G.L Sawyer, R.H. (1993). Region-specific patterns of / -keratin expression during avian development. Deo. Dynamics, 196, 283-90. 

Table 2. SAXS and XRD comparison of liquid-crystal and crystal during avian development...

Example Crippen and Snow reported their success in developing a simplified potential for protein folding. In their model, single poin Ls rep resell t am in o acids. For th e avian pan creatic polypeptide, th c n ative structure is not at a poten tial m in imum. However, a global search fotin d that the most stable poten tial m in im urn h ad only a 1.8, An gstrom root-m ean-square deviation from thenative structu re. 

The lupinane group has not attracted chemists as a primary material for modification in the hope of developing substances of possible therapeutic interest. Liberalli found lupanine was inactive in avian malaria and Clemo and Swan state that this is also the case for ll-(e-diethylamino- -pentyl)aminolupinane. Lupinine -aminobenzoate has been investigated in Russia and shown to possess marked local anaesthetic action. ... 

An interesting feature of the influenza virus sialidase active site that offers the potential for developing inhibitors specific for N1 sialidases, including avian influenza A/H5N1 virus sialidase, has recently been revealed by X-ray crystallography. The... 

Cinatl J Jr, Michaelis M, Doerr HW (2007b) The threat of avian influenza A (H5N1). IV. Development of vaccines. Med Microbiol Immunol 196 213-225 Colman PM (1994) Influenza virus neuraminidase structure, antibodies, and inhibitors. Protein Sd 3 1687-1696... 

The balance between excess and insufficient zinc is important. Zinc deficiency occurs in many species of plants and animals, with severe adverse effects on all stages of growth, development, reproduction, and survival. In humans, zinc deficiency is associated with delayed sexual maturation in adolescent males poor growth in children impaired growth of hair, skin, and bones disrupted Vitamin A metabolism and abnormal taste acuity, hormone metabolism, and immune function. Severe zinc deficiency effects in mammals are usually prevented by diets containing >30 mg Zn/kg DW ration. Zinc deficiency effects are reported in aquatic organisms at nominal concentrations between 0.65 and 6.5 pg Zn/L of medium, and in piscine diets at <15 mg Zn/kg FW ration. Avian diets should contain >25 mg Zn/kg DW ration for prevention of zinc deficiency effects, and <178 mg Zn/kg DW for prevention of marginal sublethal effects. 

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

In ovo exposure to dioxins is associated with development of grossly asymmetric avian brains, especially the forebrain and tectum. Brain asymmetry was observed in herons, cormorants, eagles, and chickens exposed to 2,3,7,8-TCDD under controlled conditions. Asymmetry appears with increasing frequency and severity in embryos and hatchlings exposed to increasing doses of... 

For avian wildlife, data are incomplete on PAH background concentrations and on acute and chronic toxicity. Studies with mallard embryos and PAHs applied to the egg surface showed toxic and adverse sublethal effects at concentrations between 0.036 and 0.18 pg PAH/kg whole egg (Hoffman and Gay 1981). Additional research is needed on petroleum-derived PAHs and then-effects on developing embryos of seabirds and other waterfowl. There is an urgent need for specific avian biomarkers of PAH exposure (Murk et al. 1996). 

The neuramidase inhibitor oseltamivir phosphate was discovered by Gilead Sciences and developed by Roche Pharmaceuticals under the name of Tamiflu (Scheme 5.13) to be used as an orally active antiviral compound for prevention and treatment of influenza infections. Because of the recent emergence of the avian flu, the demand for Tamiflu has gained momentum. Two industrially feasible syntheses are known, starting from (—)-shikimic acid and (—)-quinic acid, respectively (Scheme 5.13) [45]. 

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