Studies in the diagnosis of mineral deficiency; manganese deficiency in wheat

At fourteen sites where winter wheat was growing commercially, twelve of which were known or suspected to be deficient in manganese, a spray of manganese sulphate was applied late in the shooting stage of development, and the effect on yield of grain estimated. Samples of certain organs of unsprayed wheat plants were gathered on three occasions between tillering and ear emergence, and samples of weed leaves on the same occasions and after harvest; these samples were analysed spectrographically for manganese.
The results indicate that analysis of the wheat plant can be used to forecast its response to a manganese sulphate spray, and the following tentative limiting values for manganese content are put forward, above which no increase in grain yield as a result of treatment may be expected: (a) during tillering, 34 p.p.m. manganese in dry matter of lower leaf blades; (b) just prior to ear emergence, 36 p.p.m. manganese in dry matter of stems. The highest correlation obtained between response and manganese content was that with the values for stem samples gathered just prior to ear emergence.
Analysis of weed samples can only be expected to indicate gross differences in the manganese status of different sites.     

Pathological consequences of copper deficiency and cobalt deficiency

Aspects of the pathology of copper deficiency in several species, and cobalt deficiency in sheep, are summarized. An attempt is made to interpret morphological changes in copper-deficient animals in terms of biochemical defects. The common denominator may be mitochondrial lesions, with a generalized effect on energy-dependent synthetic functions of the cell. In copper deficiency, such defects can be attributed to depletion of copper-dependent enzymes, while deficiency of cobalt in ruminants is, in effect, deficiency of vitamin B12. The pathological consequences of vitamin B12 deficiency form a syndrome, notable features of which are neurological and muscular lesions, in which the metabolic consequences of hepatic damage may play a significant role.     

Mineral deficiency symptoms of the oil palm

Summary Young oil palms in sand culture experiment developed symptoms of nitrogen, potassium and magnesium deficiencies involving a homogeneous yellowing, a marginal yellowing and an orange chlorosis respectively. All these deficiencies resulted in poor growth and a reduced root development. A further experiment showed that Little Leaf Disease was caused by boron deficiency. Magnesium and potassium deficiency symptoms were also induced in this experiment. Sulphur deficiency symptoms, consisting of a yellowing of the young leaves, an interveinal chlorosis and necrosis, were induced in a factorial sand culture experiment and a second missing element trial. Insufficient available nitrogen, potassium, magnesium and boron all have an adverse effect on the production of inflorescences.It is considered that Plant Failure disease is caused by a poorly developed rooting system which may result from magnesium, boron and, possibly, potassium deficiencies.No evidence has been obtained to support the view that Confluent Orange Spotting is caused by potassium deficiency.     

IGF-I deficiency due to GH receptor deficiency.

IGF-I deficiency may be primary due to defective synthesis, or secondary to GH receptor deficiency (GHRD) or defects in transduction of the GH-GHR signal. Cloning and sequencing of the GHR led to recognition that circulating GH binding protein (GHBP) was structurally identical to the extra-cellular domain of the GHR, and the identification of 33 mutations of the GHR in approximately half of the 250 patients that have been reported. This review explores the information provided about GHR function by various mutations, the population distribution of GHRD, the effects of this condition on mortality, growth, development, and metabolism, the effects of replacement therapy with recombinant human IGF-I, diagnostic issues, and the question of partial GH resistance.     

ATP-citrate lyase deficiency in the mouse

ATP-citrate lyase (Acly) is one of two cytosolic enzymes that synthesize acetyl-coenzyme A (CoA). Because acetyl-CoA is an essential building block for cholesterol and triglycerides, Acly has been considered a therapeutic target for hyperlipidemias and obesity. To define the phenotype of Acly-deficient mice, we created Acly knockout mice in which a beta-galactosidase marker is expressed from Acly regulatory sequences. We also sought to define the cell type-specific expression patterns of Acly to further elucidate the in vivo roles of the enzyme. Homozygous Acly knockout mice died early in development. Heterozygous mice were healthy, fertile, and normolipidemic on both chow and high fat diets, despite expressing half-normal amounts of Acly mRNA and protein. Fibroblasts and hepatocytes from heterozygous Acly mice contained half-normal amounts of Acly mRNA and protein, but this did not perturb triglyceride and cholesterol synthesis or the expression of lipid biosynthetic genes regulated by sterol regulatory element-binding proteins. The expression of acetyl-CoA synthetase 1, another cytosolic enzyme for producing acetyl-CoA, was not up-regulated. As judged by beta-galactosidase staining, Acly was expressed ubiquitously but was expressed particularly highly in tissues with high levels of lipogenesis, such as in the livers of mice fed a high-carbohydrate diet. beta-Galactosidase staining was intense in the developing brain, in keeping with the high levels of de novo lipogenesis of the tissue. In the adult brain, beta-galactosidase staining was in general much lower, consistent with reduced levels of lipogenesis; however, beta-galactosidase expression remained very high in cholinergic neurons, likely reflecting the importance of Acly in generating acetyl-CoA for acetylcholine synthesis. The Acly knockout allele is useful for identifying cell types with a high demand for acetyl-CoA synthesis.