Development, delayed

Varieties which were intermediate in hardiness either had no significant yield depressions, or had a lighter crop than usual. In these varieties there was significant leaf death which will have delayed development in the growing season. 

Initiate therapy to treat the acute gout attack without delay. Develop a plan to assess this therapy after 24 and 48 hours. 

Intermediate-duration oral exposure to Durad 110 produced deaths in chickens associated with the delayed development of neuropathy at dosage levels of 4,000 mg/kg/day in a 28-day study and 90 mg/kg/day in a 90-day study (FMC 1986). At 100 mg/kg/day over a 13-week period, 2 of 12 male and 1 of 12 female rats died with exposure to tri- -butyl phosphate (Healy et al. 1995). Dietary administration of Pydraul 90E for 90 days providing daily doses of 50 mg/kg/day produced no chemical-related deaths in rats (Monsanto 1979). An organophosphate ester hydraulic fluid designated MIL-H-83306 also caused death in 4 of 4 rats exposed by gavage to 1,000 mg/kg over a 26-day period (Mattie et al. 1993). 

A few infants have been treated with antagonists of the NMDA receptor, an excitatory glutamatergic receptor for which glycine is a co-agonist (see Ch. 15) [29], Ketamine and dextromethorphan have been used with inconclusive results. Some infants may have had an improvement of their irritability and electroencephalogram. One infant, treated with both benzoate and dextromethorphan, was seizure-free by 12 months of age and had only moderately delayed development. However, this favorable experience has not always been duplicated. Treatment with dextromethorphan at the recommended dosage (maximum 5mg/kg/day) seems to be well-tolerated. 

Lead-zinc mixtures were more-than-additive in toxicity to marine copepods (Verriopoulos and Dimas 1988) and significantly delayed development of mud crab (Rithropanopeus harrissii) larvae (USEPA 1987). Lead is accumulated up to 10 times more rapidly by marine fishes at elevated zinc concentrations in seawater (Eisler 1981). 

Herkovits, J. and C.S. Perez-Coll. 1990. Zinc protection against delayed development produced by cadmium. Biol. Trace Elem. Res. 24 217-221. 

Depressed growth and delayed development in eye and vaginal opening during first 12 weeks all normal at necropsy after 15 weeks (Talamantes and Jang 1977)... 

Rat (Sprague- Dawtey) 11d Gd 6-16 (GO) 100 500 (delayed development, details not provided) Weeks etal. 1979... 

In many cases, UPD likely has no effect on health or development. Because most genes are not imprinted, it doesn t matter if a person inherits both copies from one parent instead of one copy from each parent. In some cases, however, it does make a difference whether a gene is inherited from a person s mother or father. A person with UPD may lack any active copies of essential genes that undergo genomic imprinting. This loss of gene function can lead to delayed development, mental retardation, or other medical problems. 

Carbon tetrachloride was fetotoxic to rats when administered on days 6-15 of gestation at 300 or 1000 ppm, 7 hours/day an increase in skeletal anomalies due to delayed development was observed in the offspring. Signs of maternal toxicity included weight loss and hepatic damage. ... 

The LCso in mice for 60 minutes was 150 ppm effects were irritation of the eyes and nose and the delayed onset of labored breathing and lethargy autopsy findings included marked pulmonary congestion and hemorrhage. Mice exposed to sublethal concentrations had pulmonary irritation and delayed development of focal necrosis in the liver and kidneys. ... 

Developmental effects in animals, consisting of resorptions, delayed development, and increased incidences of soft tissue anomalies. 

Mobley SA, Taylor DH, Laurie RD, et al. 1990. Chlorine dioxide depresses T3 uptake and delays development of locomotor activity in yoimg rats. In Jolley RL, Bull RJ, Davis WP, et al., eds. Water chlorination chemistry, environmental impact and health effects. Vol. 6. Chelsea, MI Lewis Publications, 347-358. 

Trimethoprim-sulfamethoxazole (TMP-SMX) was introduced as a fixed dose combination in 1968. Trimethoprim was added to sulfamethoxazole to synergisti-cally and sequentially inhibit bacterial synthesis of tetrahydrofolic acid. The combination was also designed to delay development of bacterial resistance. Sulfamethoxazole was selected in part because it is a congener of the frequently used sulhsoxazole but exhibits slower enteric absorption and urinary excretion. Sulfamethoxazole has a half-life similar to that of trimethoprim. 

Subtle changes that could be attributed to delayed development, such as poorly defined optic or otic placode borders (Fig. 14b, arrow) or mesencephalic flexure appearing less full in the area (Fig. 14b, circle), are assigned a score of 4. 

An exception is perfluoro(2-methylpropene) (perfluoroisobutylene, PFIB), which is the most toxic fluorinated species known so far and is particularly dangerous due to delayed development of lethal lung edema, not starting until 1-2 days after the cessation of the exposure. 

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