Meat diets and fragile bones: Inferences about osteoporosis

Because women supplemented with copper have improved bone density and femurs of rats deficient in copper have decreased mechanical strength, the hypothesis that mice fed meat would have fragile bones was tested. Mice fed sirloin are hypercholesterolemic in comparison to mice fed meat and beef liver because of a relative deficiency of copper compared to zinc. Male, albino, Swiss mice were fed trimmed sirloin or sirloin supplemented with beef liver (3/1 by weight). After 62 days, when hypercholesterolemia was detected, mice were killed and femurs were removed, cleaned and dried. Breaking strength was measured carefully at room temperature. The meat diet produced femurs 23% weaker (8.8 +/- 0.70 N/mg.100 vs 11.4 +/- 0.92, mean +/- SE, p < 0.04) in comparison to meat plus liver. Calcium, copper and phosphorus concentrations were unaffected but zinc was mildly elevated in the weak bones (426 +/- 17.5 pg/g vs 355 +/- 9.23, p < 0.002). These elements generally are unaltered in osteoporotic bones. Because copper deficiency produces osteoporosis in animals and people and because the Western diet often is low in copper, further tests of the hypothesis that diets low in copper contribute to osteoporosis are warranted.     

Renal parathyroid hormone-dependent adenylate cyclase activity after repletion of vitamin D-deficient rats with vitamin D-2

Rats fed a diet deficient in both vitamin D and Ca²⁺ exhibited a greater depression of the renal parathyroid hormone (PTH)-dependent adenylate cyclase than was observed in rats fed diets deficient in either vitamin D or calcium. Total serum Ca²⁺ was decreased from a control level of 11.2 mg/dl to 8.5 mg/dl in rats fed the diet deficient in calcium alone, and to 5.4 mg/dl in rats fed the diet deficient in vitamin D. Serum calcium was decreased further to 4.3 mg/dl in rats fed the diet deficient in both vitamin D and Ca²⁺. Serum immunoreactive PTH was significantly elevated over control levels when rats were fed the test diets; however, there were no significant differences between the elevated levels in the three experimental groups. Repletion of rats deficient in vitamin D only with a single oral dose of 3200 I.U. vitamin D-2 resulted in restoration of serum calcium to normal levels, a return of serum PTH to the control state, and an associated increase in PTH-dependent adenylate cyclase activity to the control level by 72 h. Repletion of rats deficient in both vitamin D and Ca²⁺ with the same dose of vitamin D-2 raised serum Ca²⁺ to 7.2 mg/dl by 72 h, but did not cause a reduction in circulating PTH, nor did it result in any significant improvement in the responsiveness of the membrane adenylate cyclase to PTH. These results suggest that elevated PTH is a factor in the down regulation of the PTH-dependent adenylate cyclase, but do not rule out a role for calcium as a regulatory factor.     

Studies on the application of iron to some glasshouse vegetables grown in soilless culture

Summary The application of iron to some glasshouse crops in soilless culture was studied in the course of an investigation. The growing systems consisted of nutrient film technique and rockwool. The test crops were tomatoes, cucumbers and sweet peppers.Various iron chelates were compared in a range of concentrations in a nutrient film system as well as in a rockwool system. The results showed that higher iron levels in the nutrient solution are required in the nutrient film technique than in the rockwool system. The level of the iron content in the nutrient solution had a significant effect on the structure of the root system. Crop analyses showed that on the whole no clear relationship could be found between the iron content of the plant tissues and iron chlorosis in the crop. Only in a few instances could a relationship be established and them only by averaging the results of a series of samplings.     

Sclerophylly: Evolutionary advantage or mere epiphenomenon?

ABSTRACT

The possible functional significance of sclerophylly (hard and coriaceous leaves) is discussed on the basis of different interpretations reported in old and recent literature. These, have been schematically divided into four groups of hypotheses, i.e. the “water conservation?d hypothesis, the “resistance to negative turgour pressures?d hypothesis, the “nutritional?d hypothesis and the “protective?d hypothesis. In particular, a section is devoted to discussing the first and second hypotheses in terms of relationships of sclerophylly to drought resistance strategies. Data reported in the literature lead to the conclusion that the sclerophyllous habitus per se seems not to be related to drought resistance of plants as previously thought. Nor do clear-cut relationships appear to exist between leaf sclerification and living leaf cells with thicker walls, leading to a high modulus of elasticity (ε), the latter known to be of importance for generating low leaf water potentials, i.e. higher driving forces for water uptake. Because leaf sclerification has proved to be related to soil nutrient deficiency, this leaf habitus can be considered as a mere epiphenomenon of nutrient stress. On the other hand, the selective advantage of sclerophylly as protection against herbivore attacks, though not demonstrated in different environments, seems to be of great interest and deserves further studies.     

Iron deficiency anemia induces postural control disorders in young women

BackgroundDue to menstruation and restrictive dietary practices, women are at a particular risk of iron deficiency anemia (IDA). This hematologic manifestation could impair postural control as it induces fatigue, muscle weakness, cognitive and neurological functions alteration.AimThis study aimed to investigate IDA effects on postural control in young women in comparison to healthy counterparts.Material and methodsTwenty-four young women with IDA and twenty-four controls participated in this study. Center of pressure (CoP) excursions, in the bipedal and semi-tandem postures on the firm and foam surfaces in the eyes opened (EO) and closed (EC), were recorded, and Romberg index was calculated to evaluate postural control. Besides physical performance, attentional capacity, fatigue, and heart and respiratory rates were assessed.ResultsYoung women with IDA had significantly higher CoP velocity (CoPv) values in the bipedal posture in both vision and surface conditions (EO [firm: P < 0.001 and foam: P < 0.01]; EC: P < 0.001), as well as in the semi-tandem posture (EO [firm: P < 0.01 and foam: P < 0.001]; EC: P < 0.001) compared to controls indicating that they had worse postural control than their peers. In addition, values of the respiratory rate (P < 0.001), attentional capacity (P < 0.001), physical performance (P < 0.001), fatigue (P < 0.001), and Romberg index on the foam surface in both postures (P < 0.05) were significantly higher in young women with IDA compared to controls.ConclusionsPhysical performance, fatigue, tachypnea and attentional capacity resulting from IDA may explain postural control disorder in young women.     

Purification,cellular levels,and functional domains of lipase maturation factor 1

Over a third of the US adult population has hypertriglyceridemia, resulting in an increased risk of atherosclerosis, pancreatitis, and metabolic syndrome. Lipoprotein lipase (LPL), a dimeric enzyme, is the main lipase responsible for TG clearance from the blood after food intake. LPL requires an endoplasmic reticulum (ER)-resident, transmembrane protein known as lipase maturation factor 1 (LMF1) for secretion and enzymatic activity. LMF1 is believed to act as a client specific chaperone for dimeric lipases, but the precise mechanism by which LMF1 functions is not understood. Here, we examine which domains of LMF1 contribute to dimeric lipase maturation by assessing the function of truncation variants. N-terminal truncations of LMF1 show that all the domains are necessary for LPL maturation. Fluorescence microscopy and protease protection assays confirmed that these variants were properly oriented in the ER. We measured cellular levels of LMF1 and found that it is expressed at low levels and each molecule of LMF1 promotes the maturation of 50 or more molecules of LPL. Thus we provide evidence for the critical role of the N-terminus of LMF1 for the maturation of LPL and relevant ratio of chaperone to substrate.     

Identification of rare variants causing urea cycle disorders: A clinical,genetic, and biophysical study

Urea cycle disorders (UCDs) are a group of rare metabolic conditions characterized by hyperammonemia and a broad spectrum of phenotypic severity. They are caused by the congenital deficiency in the eight biomolecules involved in urea cycle. In the present study, five cases of UCD were recruited and submitted to a series of clinical, biochemical, and genetic analysis with a combination of high throughput techniques. Moreover, in silico analysis was conducted on the identified missense genetic variants. Various clinical and biochemical indications (including profiles of amino acids and urinary orotic acids) of UCD were manifested by the five probands. Sequence analysis revealed nine diagnostic variants, including three novel ones, which caused Argininosuccinic aciduria (ASA) in one case, Carbamoyl phosphate synthetase 1deficiency (CPS1D) in two cases, Ornithine transcarbamylase deficiency (OTCD) in one case, and Citrin deficiency in 1case. Results of in silico biophysical analysis strongly suggested the pathogenicity of each the five missense variants and provided insight into their intramolecular impacts. In conclusion, this study expanded the genetic variation spectrum of UCD, gave solid evidence for counselling to the affected families, and should facilitate the functional study on the proteins in urea cycle.     

An Unusual Cause of Renal Amyloidosis Secondary to Gout—the First Description of Familial Occurrence

Background: AA amyloidosis caused by the chronic inflammation accompanying gouty arthritis is extremely rare and familial occurrence has not been described so far. Case report: We present the case of two brothers (47 and 44 years old) with 7- and 10-year history of hyperuricaemia and chronic tophaceous gout with polyarticular involvement. The enzymatic assay performed in their erythrocytes proved the partial hypoxanthine-guanine phosphoribosyl transferase deficiency (Kelley-Seegmiller syndrome), the genetic defect of purine metabolism. Later on they developed proteinuria and chronic renal insufficiency /CRI/. Renal biopsy disclosed the combination of AA amyloidosis and gouty nephropathy in both the cases. Despite the standard treatment the older brother progressed to chronic renal failure. On the contrary, the younger one being longterm treated with oral colchicin have stabilized CRI. Conclusions: Only several cases of AA renal amyloidosis until recently, secondary to gout have been reported. Our case represents the first report of familial occurrence of this extremely rare disease.     

Contribution of the α8 Integrin Chain to the Expression of Extracellular Matrix Components

Abstract

In the kidney, the α8 integrin chain (itga8) is expressed in mesenchymal cells and is upregulated in fibrotic disease. We hypothesized that itga8 mediates a profibrotic phenotype of renal cells by promoting extracellular matrix and cytokine expression. Genetic itga8 deficiency caused complex changes in matrix expression patterns in mesangial and smooth-muscle cells, with the only concordant effect in both cell types being a reduction of collagen III expression. Silencing of itga8 with siRNA led to a decline of matrix turnover with repression of matrix metalloproteinases and reduction of matrix production. In contrast, de novo expression of itga8 in tubular epithelial cells resulted in reduced collagen synthesis. Overexpression of itga8 in fibroblasts did not change the expression of matrix molecules or regulators of matrix turnover. Thus, the influence of itga8 on the expression of matrix components was not uniform and celltype dependent. Itga8 seems unlikely to exert overall profibrotic effects in renal cells.