My Newborn Life In A Harem.rar

In establishing the protein requirements at different stages of life, three factors must be considered: (1) energy concentration in the diet, (2) amino acid composition of the protein (see Appendix Table 2), and (3) bioavailability of the amino acids.

Protein deficiency in young rats results in reduced growth, anemia, hypoproteinemia, depletion of body protein, muscular wasting, emaciation, and, if sufficiently severe, death. In adults a loss of weight and body nitrogen occurs (Cannon, 1948), and chronic deficiency may lead to edema (Alexander and Sauberlich, 1957). Estrus becomes irregular and may cease, fetal resorption occurs, and newborns are weak or dead. A lack of protein for pregnant and lactating rats may result in offspring that are stunted in growth (Hsueh et al., 1967) and have reduced concentrations of DNA and RNA in various tissues (Zeman and Stanbrough, 1969; Ahmad and Rahman, 1975). Low-protein diets also result in reduced food intake (Black et al., 1950). The reproductive capacity of the male is impaired by consumption of diets with inadequate concentrations of protein (Goettsch, 1949).

Vitamin D is an important precursor of the hormone 1,25-dihydroxycholecalciferol. The hormonal action is mediated by the interaction with a specific nuclear receptor and the corresponding responsive elements in the promotor regions of the genes that code for several proteins, many of which are involved in calcium metabolism. Although 1,25-dihydroxycholecalciferol is best known for its role in the regulation of calcium and phosphorus homeostasis, it may have significant roles in many other processes, including the synthesis of red blood cells, the proliferation of B and T lymphocytes, and the secretion of insulin and prolactin (Reichel et al., 1989). Vitamin D is hydroxylated in two positions before it becomes active. First, cholecalciferol is converted to 25-hydroxycholecalciferol in the liver. In the kidney 25-hydroxycholecalciferol is hydroxylated to form the active 1,25-dihydroxycholecalciferol. The formation of 1,25-dihydroxycholecalciferol is a tightly regulated process. Serum calcium concentration regulates the activity of the kidney 1-α-hydroxylase enzyme via the parathyroid gland. Low concentrations of serum phosphate directly increase the synthesis of this kidney enzyme. High dietary concentrations of both cause a decrease in the formation of 1,25-dihydroxycholecalciferol.

In mammals, vitamin B12 is required as a coenzyme for the transmethylation of homocystine to methionine, in utilizing 5-methyl-tetrahydrofolic acid, and in the conversion of methylmalonyl-CoA to succinyl-CoA (Weissbach and Taylor, 1970). The concentration of vitamin B12 needed in the diet of the rat may vary with dietary content of choline, methionine, and folic acid. A number of conditions have been reported that impair vitamin B12 absorption. Rats fed a diet with raw kidney bean (Phaseolus vulgaris) as 4 percent of dietary protein or 0.5 percent phytohemagglutinin developed vitamin B12 malabsorption after only 3 days, and the condition was not correctable by giving intrinsic factor (Banwell et al., 1980). Highly fermentable fibers such as pectin, guar gum, and xylan fed as 5 percent of the diet increased urinary methylmalonic acid and depressed the oxidation of propionate to CO2 (Cullen and Oace, 1989a). The half-life of vitamin B12 was 58 days for rats fed fiber-free diets and 38 days for rats fed a 5 percent pectin diet (Cullen and Oace, 1989b). Vitamin B12 deficiency has been induced by diets containing unheated soybean flour, but amino acid deficiencies occur also and unheated soybean flour contains other toxins; therefore, it has been suggested that its use for the study of vitamin B12 deficiency is not justified (Edelstein and Guggenheim, 1971; Williams and Spray, 1973). Giardiasis also has been reported to impair vitamin B12 absorption (Deka et al., 1981). The oxidation of acetaldehyde, generated from the metabolism of ethanol, by xanthine oxidase inhibited the ability of vitamin B12 to bind to intrinsic factor (Shaw et al., 1990). Decreased vitamin B12 concentrations have been reported in rats fed liquid diets with ethanol but not natural-ingredient diets with ethanol (Frank and Baker, 1980). Hypothyroidism slowed the rate of depletion of hepatic vitamin B12 (Stokstad and Nair, 1988). Vitamin B12 deficiency developed rapidly in rats exposed to nitrous oxide (Horne and Briggs, 1980; Muir and Chanarin, 1984).

Signs of Choline Deficiency Choline deficiency appears much more rapidly in male than in female rats (Patek et al., 1969). Droplets of triglycerides and abnormalities of the intracellular membranes appear in the livers of weanling male rate within 24 hours after they have ingested a choline-deficient diet. Long-term deficiency leads first to fatty liver, in which triglycerides may compose as much as 50 percent of the total wet weight of the liver and the liver cells are markedly distended with fat vacuoles, and then to cirrhosis, in which there is proliferation of fibrovascular tissue, vascular shunting, and hepatic failure (Zaki et al., 1963; Rogers and MacDonald, 1965). Sucrose was found to cause twice as great an increase in liver triglycerides as dextrin in choline-deficient diets (Chalvardjian and Stephens, 1970).

Signs of Riboflavin Toxicity Excessive concentrations of dietary riboflavin have been shown to decrease survivability of newborn rat pups. Mortality during the first week of life was increased 19 percent in a strain of Long-Evans rats by increasing the concentration from 6 to 12 mg/kg (Eckhert, 1987), and the percent of newborn Sprague-Dawley rats surviving to weaning was reduced 7 percent by increasing riboflavin from 8 to 80 mg/kg (Shirley, 1982). Chronic intakes of 12 mg/kg have been shown to cause photoreceptor damage (Eckhert et al., 1989, 1991).

Signs of Thiamin Deficiency Thiamin deficiency can be induced readily and produces anorexia and weight loss with an increase in food spillage (Tagliaferro and Levitsky, 1982) and in coprophagy (Fajardo and Hornicke, 1989). Thiamin-deficient rats avoid eating sucrose (Yudkin, 1979) and are slower to respond to tasks where food pellets are used for reinforcement (Hashimoto, 1981). Evaluations of behavior demonstrated that rats maintained on thiamin-deficient diets showed muricide aggression (Onodera et al., 1981; Onodera, 1987). After 7 days of deficiency there is a decrease in white and red blood cells and a drop in hemoglobin. After 30 days this is reversed and reticulocytes and plasma erythropoietin are increased, but red blood cell 2,3-diphosphoglycerate, membrane cholesterol, and phospholipids decrease (Hobara and Yasuhara, 1981). After 4 weeks there is a decrease in liver thiamin and an elevation in plasma branched-chain amino acids, α-ketoacids, and α-hydroxyacids (Shigematsu et al., 1989). Deficiency during pregnancy resulted in intrauterine growth retardation (Roecklein et al., 1985) and decreased activity of the thiamin-dependent enzymes pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and transketolase (Fournier and Butterworth, 1990) and gangliosides (Vaswani, 1985) in newborn rat brains. Acetylcholine was reduced in weanling rats of thiamin-deficient mothers (Kulkarni and Gaitonde, 1983).

Because vanadium is known to be required by some haloperoxidases in lower life forms (Yu and Whittaker, 1989), it has been suggested that peroxidases involved in iodine metabolism in animals may be vanadium-dependent. Some studies have attempted to show an interaction between iodine and vanadium, but the findings were inconclusive and more definitive experiments have not been forthcoming (Uthus and Nielsen, 1990). Because of the lack of definitive and repeatable experiments on the nutritive response to vanadium, its essentiality for the rat or other mammals is uncertain.

Arata has a carefree and cheerful personality who is usually bantering and teasing others even in dangerous situations. He is also noted to be very perverted, often finding himself in risque situations or confessing his desires towards a girl. Usually, this is by complete accident, but he simply rolls with it and lets himself enjoy the situation without getting worked up about it. During these situations, he usually quotes: "Thank you for the treat" or something to that effect. This often earns him a scolding from Lilith Asami and scorn from Mira Yamana, the Top Seat of Grimoire Security, who calls him filthy or impure. Other girls such as Levi Kazama, Akio Fudo or Lieselotte Sherlock don't particularly mind and often goes along with his remarks. However, he knows where to draw the line, as he refuses a kiss from Yui Kurata because that is only for "when we're closer". In times of need, Arata can become very dependable. He is very calm under pressure, in both perverted and dangerous situations. His natural way of thinking allows him to make rational decisions and develop solutions to problems that would cause others to panic. Arata cares very deeply for others, especially his friends. He is willing to risk his life and become stronger to save those he cares about, such as Lillith, Yui, Lieselotte, etc.

Born into a normal family despite being a Demon Lord Candidate, Arata lived an ordinary life until the death of his parents due to a plane crash of unknown cause at a young age. As a result, he would live together with his cousin Hijiri and her family. During elementary school, the two would develop a close bond with each other as Arata was the only one who treated her kindly despite not knowing she was a Magus.

Much Later Anastasia-L transferred her reincarnation magic to him which allowed him relieve a new life. This magic is extremely useful as it helps someone escape death. This magic activates automatically upon Anastasia-L process of disappearance. Since it's Anastasia-L own life, the reincarnated will reincarnate in their own life style. This is probably the reason why Arata reincarnated as a child. 781b155fdc