Effects of cadmium in herbage on the apparent absorption of elements by sheep in comparison with inorganic cadmium added to their diet

A meta-analysis of existing scientific literature recently suggested that Cd is absorbed more efficiently by sheep if it is in the organic form in grass, than if it is added as an inorganic supplement to the diet. We tested this experimentally by feeding sheep grass from contaminated soil, compared with uncontaminated grass and with Cd added to the diet. To produce contaminated herbage, Cd nitrate was added to soil in 11 lysimeters sown with perennial ryegrass, with a further 11 lysimeters receiving no Cd to produce uncontaminated herbage. In the Cd-treated lysimeters, soil had increased exchangeable K, Mg, and Ca, leachate had increased K, Mg, Ca, Na, and P, grass had increased Cd and reduced Mg, Na, P, Mn, Fe, Cr, Al, and Ni, and there was some reduction in grass yield compared with untreated lysimeters. Grass from Cd-treated or untreated lysimeters was fed to groups of 12 ewes for 2 days, with Cd intake equated by adding Cd nitrate to the concentrate feed of ewes receiving the uncontaminated grass. The apparent absorption of Cd, Zn, Mo, Cr, and Al was increased for ewes receiving Cd-enriched grass, and apparent absorption of Cu was reduced, compared to those receiving supplementary inorganic Cd. Most of the unabsorbed Cd was excreted in feces within 4 days of feeding. The ewes consuming Cd in grass had increased B concentrations in their urine, possibly due to adverse effects of Cd on kidney function. Finally, the ewes were offered a choice of the two herbages and they ate significantly more of the uncontaminated grass. It is concluded that the apparent absorption of Cd and other heavy metals by sheep in a short-term experiment was greater when Cd was in the grass than when the Cd was added in in an inorganic form and that sheep partially avoided herbage with a high Cd concentration.     

Bone mineralization and metabolism of3H-25-hydroxyvitamin D3 in thyroparathyroidectomized rats treated with parathyroid extract

Summary Thyroparathyroidectomized rats fed a diet containing 1.2% calcium, 0.55% phosphorus maintain normal serum levels of these ions. Treatment of such rats with parathyroid extract (PTE; 20 U/100 g twice daily; 10 days) has no statistically significant effect on rates of bone formation, matrix apposition, or osteoid maturation. Significant decreases in osteoid width and mineralizing front width, as well as a 60% increase in the rate of initial mineralization were observed in the PTE-treated group. Conversion of³H-25-hydroxyvitamin D₃ to³H-1,25-dihydroxyvitamin D₃ was 4-fold higher in the PTE-treated group than in the untreated animals. Increased formation of 1,25-dihydroxyvitamin D₃ in response to treatment with PTE may play a major role in correcting the mineralizing defect resulting from thyroparathyroidectomy.     

Effect of the Proportion of Organic Material in Bone on Thermal Decomposition of Bone Mineral: An Investigation of a Variety of Bones from Different Species Using Thermogravimetric Analysis coupled to Mass Spectrometry,High-Temperature X-ray Diffraction,and Fourier Transform Infrared Spectroscopy

Thermogravimetric analysis linked to mass spectrometry (TGA-MS) shows changes in mass and identifies gases evolved when a material is heated. Heating to 600 degrees C enabled samples of bone to be classified as having a high (cod clythrum, deer antler, and whale periotic fin bone) or a low (porpoise ear bone, whale tympanic bulla, and whale ear bone) proportion of organic material. At higher temperatures, the mineral phase of the bone decomposed. High temperature X-ray diffraction (HTXRD) showed that the main solids produced by decomposition of mineral (in air or argon at 800 degrees C to 1000 degrees C) were beta-tricalcium phosphate (TCP) and hydroxyapatite (HAP), in deer antler, and CaO and HAP, in whale tympanic bulla. In carbon dioxide, the decomposition was retarded, indicating that the changes observed in air and argon were a result of the loss of carbonate ions from the mineral. Fourier transform infrared (FTIR) spectroscopy of bones heated to different temperatures, showed that loss of carbon dioxide (as a result of decomposition of carbonate ions) was accompanied by the appearance of hydroxide ions. These results can be explained if the structure of bone mineral is represented by [Formula: see text] where V(Ca) and V(OH) correspond to vacancies on the calcium and hydroxide sites, respectively, and 2-x-y = 0.4. This general formula is consistent in describing both mature bone mineral (i.e., whale bone), with a high Ca/P molar ratio, lower HPO4(2-) content, and higher CO3(2-) content, and immature bone mineral (i.e., deer antler), with a low Ca/P ratio, higher HPO4(2-), and lower CO3(2-) content.     

Bone mineral density and mortality in women and men: the NHANES I epidemiologic follow-up study

PURPOSE: We sought to assess the long-term association of bone mineral density with total, cardiovascular, and non-cardiovascular mortality. METHODS: The First National Health and Nutrition Examination Survey data were obtained from a nationally representative sample of non-institutionalized civilians. A cohort aged 45 through 74 years at baseline (1971-1975) was observed through 1992. Subjects were followed for a maximum of 22 years. Included in the analyses were 3501 white and black subjects. Death certificates were used to identify a total of 1530 deaths. RESULTS: Results were evaluated to determine the relative risk for death per 1 SD lower bone mineral density, after controlling for age at baseline, smoking status, alcohol consumption, history of diabetes, history of heart disease, education, body mass index, recreational physical activity, and blood pressure medication. Bone mineral density showed a significant inverse relationship to mortality in white men and blacks, but did not reach significance in white women. Based on 1 SD lower bone mineral density, the relative risk for white men was 1.16 (95% confidence interval (CI), 1.07-1.26, p<.01), while for white women the relative risk was 1.10 (95% CI, 0.99-1.23, p=.07), and in blacks the relative risk was 1.22 (95% CI, 1.05-1.42, p<.01). Bone mineral density was also associated with non-cardiovascular mortality in all three race-gender groups. An association between bone mineral density and cardiovascular mortality was found only in white men. CONCLUSIONS: Bone mineral density is a significant predictor of death from all causes (white men, blacks), cardiovascular (white men only) and other causes combined, in whites and blacks.     

DC元数据在数字图书馆中的应用

 

从元数据的概念入手，介绍了DC元数据的产生和发展，体系结构及其在电子资

源描述中的优势等，并从五个方面介绍了DC元数据在数字图书馆中的应用，包括信息资源的

组织，解决系统互操作问题，为用户实现知识导航，用户管理，数据库的设计与维护。

     

Mineral and bone physiology in the foetus,preterm and full-term neonates

Mother is the major source of minerals in foetal life with placenta actively transporting against a concentration and electrochemical gradient. The foetal serum mineral concentration is thereby higher as compared to maternal values, which possibly help in its rapid accretion in developing bones and for counteracting postnatal fall in calcium levels at birth. Parathyroid hormone related peptide (PTHrP) and parathyroid hormone (PTH) play a major role in mineral physiology during foetal life with hormones like calcitriol, calcitonin, FGF-23 and sex steroids having minimal role. PTHrP and PTH also play a major role in endochondral bone formation and mineralization of skeleton. At the birth, as the cord is clamped, there is loss of active transport of minerals through placenta and the neonate has to rely on enteral intake of minerals to meet the demands of growing bones and metabolisms. The calcium levels fall after birth, reaching a nadir at 24–48 h and gradually rise to adult values over several days, probably resulting from a fall in PTHrP levels and hyporesponsiveness of parathyroid glands. As PTH and calcitriol levels increase postnatally, there is a rise in calcium levels with maturation in functioning of kidneys and intestines. However, there may be significant delay in intestinal maturation in preterm infants along with an increased demand for mineral accretion, which predispose them to osteopenia of prematurity.     

Chronic Alcohol Consumption Disrupted Cholesterol Homeostasis in Rats: Down‐Regulation of Low‐Density Lipoprotein Receptor and Enhancement of Cholesterol Biosynthesis Pathway in the Liver

Background: Chronic alcohol consumption causes alcoholic liver disease, which is associated, or initiated, with dysregulated lipid metabolism. Very recent evidence suggested that dysregulated cholesterol metabolism plays an important role in the pathogenesis of alcoholic fatty liver diseases, however, the effects of chronic alcohol exposure on cholesterol homeostasis have not been well studied and underlying mechanisms behind are still elusive. Methods: Male Sprague–Dawley rats weighing 250 ± 5.5 g (mean ± SEM) divided into 2 groups (8 rats per group) and pair‐fed with liquid diets containing (in percent of energy intake) 18% protein, 35% fat, 12% carbohydrate, and 35% either ethanol (ethanol diet) or an isocaloric maltose‐dextrin mixture (control diet), according to Lieber and De Carli, for 4 weeks. Results: Long‐term excessive alcohol feeding to rats caused fatty liver and liver injury, which was associated with disrupted cholesterol homeostasis, characterized by increased hepatic cholesterol levels and hypercholesterolemia. Hepatic cholesterol increases were concomitant with constantly activated sterol regulatory element‐binding protein‐2 (SREBP‐2) in the liver and increased expression of 3‐hydroxy‐3‐methyl‐glutaryl‐CoA (HMG‐CoA) reductase, a rate‐limiting enzyme for cholesterol de novo synthesis, indicating enhanced cholesterol biosynthesis. Alcohol‐induced hypercholesterolemia was accompanied by decreased LDL receptor (LDLr) levels in the liver. Further investigations revealed that chronic alcohol exposure increased hepatic proprotein convertase subtilisin/kexin type 9 (PCSK9) contents to down‐regulate LDLr via a post‐translational mechanism. Moreover, alcohol feeding suppressed extracellular signal‐regulated kinase (ERK) activation in the liver. In vitro studies showed that inhibition of ERK activation was associated with decreased LDLr expression in HepG2 cells. Conclusions: Our study provides the first evidence that both increased PCSK9 expression and suppressed ERK activation in the liver contributes to alcohol‐induced hypercholesterolemia in rats.     

The effect of the microscopic and nanoscale structure on bone fragility

Bone mineral density is the gold-standard for assessing bone quantity and diagnosing osteoporosis. Although bone mineral density measurements assess the quantity of bone, the quality of the tissue is an important predictor of fragility. Understanding the macro- and nanoscale properties of bone is critical to understanding bone fragility in osteoporosis. Osteoporosis is a disease that affects more than 75 million people worldwide. The gold standard for osteoporosis prognosis, bone mineral density, primarily measures the quantity of bone in the skeleton, overlooking more subtle aspects of bone's properties. Bone quality, a measure of bone's architecture, geometry and material properties, is evaluated via mechanical, structural and chemical testing. Although decreased BMD indicates tissue fragility at the clinical level, changes in the substructure of bone can help indicate how bone quality is altered in osteoporosis. Additionally, mechanical properties which can quantify fragility, or bone's inability to resist fracture, can be changed due to alterations in bone architecture and composition. Recent studies have focused on examination of bone on the nanoscale, suggesting the importance of understanding the interactions of the mineral crystals and collagen fibrils and how they can alter bone quality. It is therefore important to understand alterations in bone that occur at the macro-, micro- and nanoscopic levels to determine what parameters contribute to decreased bone quality in diseased tissue.     

Development of a carcinogenic potency index for dermal exposure to viscous oil products

Polycyclic aromatic compounds (PACs) present in oil streams and formulated products are important determinants of possible carcinogenicity. Following dermal exposures the transport of the PACs from oil (the carrier) into the skin is a factor that may affect macromolecular (DNA) adduct formation and thus determine carcinogenicity. We have developed a mathematical model, which describes the flux into the skin for a representative carcinogenic PAC, benzo(a)pyrene. The model is based on measurements of the amount of benzo(a)pyrene bound to skin DNA or blood observed in mouse skin painting studies. The degree of adduct formation from a particular oil product, which we term the Bioavailability Index (BI), was shown to be a function of both the viscosity of the oil product, which affected the transport of the PAC through the carrier, and the aromaticity, which affected the partition of PAC between the carrier and the skin. Literature data were analysed from mouse skin painting studies with mineral oils of known carcinogenicity. A linear relationship was shown between the amount of DNA adduct formation, expressed as alkylation frequency, and the arithmetic product of the total (3–6) ring PAC content and the BI, which we have termed the Carcinogenic Potency Index (CPI). Comparison of literature data on DNA alkylation frequencies for oil products and their carcinogenicity indicated that oils giving rise to an alkylation frequency below a certain threshold (ca. 1 adduct in 10⁸ nucleotides) are non-carcinogenic to mouse skin. This threshold level can be translated into a value for the CPI, below which the genotoxic carcinogenic risk arising from skin contact with the oil product is considered to be negligible. The CPI for bitumens is well below this value, being both due to the low BI from bitumen, but more so, due to their low PAC content. For some bitumens diluted with solvents, i.e. cutback-bitumens, the CPI may exceed this value, indicating a possible carcinogenic risk for some of the cutback-bitumens. The main determining factor is the PAC content which is principally determined by the nature of the diluent used. Received: 16 December 1998 / Accepted: 16 February 1999     

兴城矿泉浴治疗强直性脊柱炎临床疗效评价

比较在改变病情药（DMARDs）基础上用矿泉和淡水浴治疗强直性脊柱炎（AS）的疗效。方法48例AS患者随机分为矿泉浴治疗试验组和淡水浴对照组，二组水温同为38～40℃，每次30分钟，每日1次，共60次；同时均口服柳磺毗陡（SASP）第1周0．5，每日3次，第2周起1．0，每日3次及甲氨喋呤（MTX）第1周5．0mg，第2周7．5mg，第3周10mg,第4周15mg，每周1次。治疗前后对腰背痛指数、晨僵时间、夜间痛计分、外周关节痛指数、胸廓扩张度、Schober试验、血沉（ESR）、C反应蛋白（CRP）、指地距、枕墙距及骰骼关节X线改变等指标进行评价并对比分析。结果试验组总有效率（87．50％）明显高于对照组（56．25％，P＜0．05），尤其在改善夜间痛、外周关节痛、枕墙距、指地距、腰背痛、CRP及缩短晨但时间方面优于对照组（P＜0．05）。结论兴城矿泉浴在治疗AS时可对DMARDs产生协同作用。疗效优于对照组。