Advances in revolutionary technologies pose new challenges for human life; in response to them, global responsibility is pushing modern technologies toward greener pathways. Molecular imprinting technology (MIT) is a multidisciplinary mimic technology simulating the specific binding principle of enzymes to substrates or antigens to antibodies; along with its rapid progress and wide applications, MIT faces the challenge of complying with green sustainable development requirements. With the identification of environmental risks associated with unsustainable MIT, a new aspect of MIT, termed green MIT, has emerged and developed. However, so far, no clear definition has been provided to appraise green MIT. Herein, the implementation process of green chemistry in MIT is demonstrated and a mnemonic device in the form of an acronym, GREENIFICATION, is proposed to present the green MIT principles. The entire greenificated imprinting process is surveyed, including element choice, polymerization implementation, energy input, imprinting strategies, waste treatment, and recovery, as well as the impacts of these processes on operator health and the environment. Moreover, assistance of upgraded instrumentation in deploying greener goals is considered. Finally, future perspectives are presented to provide a more complete picture of the greenificated MIT road map and to pave the way for further development.

Molecular Imprinting: Green Perspectives and Strategies.

Treatment of Wilson and menkes diseases.

The chemical similarities between copper, zinc, and cadmium led to the speculation that there existed a copper component of cadmium toxicity in addition to the previously shown zinc component. Cadmium was found to be toxic to chicks at dietary levels of 25 to 400 ppM in a copper- and iron-deficient diet. The toxicity resulted in a reduced growth rate, mortality, microcytic hypochromic anemia, and atony and elongation of the gizzard. The growth depression and gizzard abnormality were corrected by increased dietary zinc. The mortality was reversed by added copper indicating that the speculation which prompted the study was valid. Increased dietary iron partially corrected both the mortality and the growth depression, indicating a previously unsuspected iron component of cadmium toxicity. 13 references, 6 tables.

In vivo interactions of cadmium with copper, zinc, and iron

Preface Demands by experimental workers for standard materials, in this case for animals of similar, stable and repeatable performance, have resulted in an increasing sophistication in laboratory animal husbandry. Microbiological and genetic definition of animals has improved reproducibility of results, but variation is still introduced or enhanced by other factors, one of the most common of which is the diet. With this in mind the Medical Research Council Laboratory Animals Centre set up in 1974 a Laboratory Animals Diets Advisory Committee. The

https://lan.sagepub.com/content/11/1/1.full.pdf

Dietary standards for laboratory animals: report of the Laboratory Animals Centre Diets Advisory Committee.

1. Six groups of four litter-mate female Large White pigs of about 17 kg live weight were allocated according to a 2×2 factorial design in each of two experiments in which rations containing 0 or 750 ppm copper were offered with either 0 and 500 ppm zinc, or 0 and 750 ppm iron. 2. Severity of toxicosis was assessed by determining aspartate transaminase activity in serum, observing the incidence of jaundice and determining the hemoglobin concentration in whole blood and Cu concentration in serum and liver. 3. Addition of 750 ppm Cu to the diet caused toxicity in nine out of twelve animals; it was most severe after about 4 weeks when two-to five-fold increases in serum Cu and aspartate transaminase levels were found and seven pigs were jaundiced. Serum Cu and aspartate transaminase concentrations and degrees of jaundice were apparently interrelated and returned to normal levels after 6 weeks, suggesting adaptation to the high Cu intake. Growth depression and a microcytic hypochromic anaemia persisted. 4. Addition of 500 ppm Zn or 750 ppm Fe in the presence of 750 ppm Cu eliminated jaundice and produced serum Cu and aspartate transaminase concentrations similar to control values after 4 weeks. Only supplementary Fe afforded protection against anaemia. 5. Variability in the response of the pig to Cu supplements could be partly due to variations in the intake of Fe and Zn. The addition of Fe and Zn supplements to pig diets supplemented with Cu would probably reduce the small risk of causing Cu poisoning.

/pdf/studies-of-the-toxicity-of-copper-to-pigs-1-effects-of-oral-2jenl5e524.pdf

Sedgwick E. Smith

Papers

Zinc toxicity in rats; antagonistic effects of copper and liver.

Further studies of manganese deficiency in the rabbit.

Studies of the manganese requirement of rabbits.