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Mortality from stomach cancer in Ontario miners.

An excess of mortality from stomach cancer has been found in Ontario gold miners (observed (obs) 104, standardised mortality ratio (SMR) 152, 95% confidence interval (95% CI) 125-185) and no excess of stomach cancer could be detected in other miners in Ontario (obs 74, SMR 102, 95% CI 80-128). The excess of stomach cancer appeared five to 19 years after the miners began gold mining in Ontario. In that interval, similar patterns of excess mortality from stomach cancer were found in miners born in north America (obs 14, SMR 268, CI 147-450) and in miners born outside north America (obs 12, SMR 280, 95% CI 145-489). Twenty or more years after the miners began mining gold, an excess of mortality from stomach cancer was found in gold miners born outside of north American (obs 41, SMR 160, 95% CI 115-218) but not in gold miners born in north America (obs 37, SMR 113, 95% CI 80-156). The excess of stomach cancer in gold miners under the age of 60 (obs 45, SMR 167, 95% CI 122-223) seems larger than the excess in gold miners between the ages of 60 and 74 (obs 59, SMR 143, 95% CI 109-184). Exposures to arsenic, chromium, mineral fibre, diesel emissions, and aluminium powder were considered as possible explanations of the excess of stomach cancer in Ontario gold miners. Exposure to diesel emissions and aluminium powder was rejected as gold miners and uranium miners were exposed to both agents but an excess of stomach cancer was noted only in gold miners. The association between the excess of stomach cancer and the time since the miner began mining gold suggested that duration of exposure to dust in gold mines ought to be weighted according to the time since the exposure to dust occurred and that an appropriate time weighting function would be one in the interval five to 19 years after each year of exposure to dust and zero otherwise. A statistically significant association between the relative risk of mortality from stomach cancer and the time weighted duration of exposure to dust in gold mines was found in miners under the age of 60. Time weighted indices of exposure to chromium and arsenic were formed for each gold miner by time weighting the product of the duration of exposure to dust in a gold mine and the percentages of arsenic and chromium in rocks in that gold mine. Exposure to mineral fibre was measured in terms of the time weighted duration of employment in those gold mines that contain mineral fibre. A statistically significant association between the excess of stomach cancer in gold miners under the age of 60 and the time weighted index of exposure to chromium occurred and not association was found between the excess of stomach cancer and either the time weighted duration of employment in mines containing mineral fibre. The excess of stomach cancer in gold miners under the age of 60 was better associated with the time weighted index of exposure to chromium than to the time weighted duration of exposure to dust in gold mines. Although the number of cases of gastric cancer that were classified according to the system of Lauren was small, the data suggest that for miners under the age of 60, exposure to chromium is associated with the development of the intestinal rather than the diffuse type of gastric cancer.

Adult↗

Endochondral mineralization in cartilage organoid culture.

In the development of secondary bone, mineralization of the cartilage matrix is the first step in endochondral mineralization. The circumstances of cartilage mineralization are not known. Influences of the periosteal tissue have been mentioned. In order to investigate the role of osteoblastic cells in endochondral mineralization, cartilage organoid cultures were induced to mineralize by the addition of beta-glycerophosphate (beta-GP). In cartilage organoid culture, embryonic mouse limb bud mesenchymal cells were grown at high-density. The cells differentiated into mature chondrocytes and produced hyaline cartilage matrix. When cartilage had formed after 6 days in vitro, 10 mM beta-GP was added. The developed mineralized cartilage was investigated by morphological means. Seven days after the addition of beta-GP, the first mineralized spots were visible mainly in the internodular, noncartilage tissue. After 12 to 14 days, large areas of cartilage were mineralized, and after 21 days, nearly the whole culture had been mineralized. Electron microscopic investigations showed a dramatic alteration of the cartilage matrix followed by a homogeneous mineralization of the cartilage matrix. The chondrocytes in the mineralized area died and faded. Typical rod-like apatite crystals were visible at the border between the mineralized and the unmineralized matrix. This result closely resembles the in vivo situation of cartilage mineralization. Addition of osteoblastic calvarial cells enhanced the mineralization process, as did the addition of conditioned medium of calvarial cell monolayers. Under these treatments, mineralization started after 3 days and reached a maximum after 14 days. On the other hand, addition of mouse skin fibroblast-like cells without a direct contact to the cartilage inhibited cartilage mineralization. These results indicate that osteoblastic cells induce endochondral mineralization, whereas fibroblast-like cells inhibit this mineralization via soluble factors.

Animals↗

Relationship between mineral distributions in dentine lesions and subsequent remineralization in vitro.

Though the mineral distribution of the dentine carious lesion varies largely from tooth to tooth and from patient to patient, there are two main distribution profiles that characterize natural carious lesions in dentine. These profiles include softened and subsurface lesion types. The mineral distribution relationship between the starting profile and the profile after remineralization is not known. In order to study the relational aspects, we have produced demineralized dentine samples in vitro with mineral profiles similar to those of typical natural carious lesions, and subsequently remineralized the samples in a remineralizing solution with various fluoride concentrations (0, 2 and 10 ppm F). The mineral distributions were obtained by using an improved microradiographic technique. In addition, the nature of deposited mineral was analyzed by diamond-coupled total internal reflectance spectroscopy. Definite relationship was observed between the original lesion mineral distribution and the mineral distributions following remineralization. The amount of mineral present in approximately the first 50 microm of the lesion influenced the overall mineral profile after remineralization, possibly through influencing ion transport. If the amount was high (> approximately 10 vol%), the deposited mineral was confined to the surface (0-50 microm). The original mineral at those depths acted like a nucleus of mineral regrowth when the amount of residual mineral was intermediate, and like a transport barrier when the surface layer was well mineralized. If a surface barrier was not present, mineral was deposited at deeper depths in the lesion. Fluoride effect on dentine remineralization was dependent on the original mineral content and its distribution in the lesion. Although a high concentration of fluoride was very effective in low-mineral lesions, it produced hyperremineralization on well-mineralized subsurface lesions so that it prevented effective remineralization especially in deeper lesions.

Acetic Acid↗

The mineralization of bone tissue: a forgotten dimension in osteoporosis research.

Osteoporosis treatment should not only prevent the loss of bone tissue, not interfere with apatite and avoid bone mineral changes at the crystal level, but should also increase the mechanical resistance of bone and thus protect the skeleton against new fractures. Mineral substance is crystallized as nonstoichiometric carbonated apatite ionic crystals of small size and extended specific surface. Consequently, they have a very large interface with extracellular fluids, and numerous interactions between ions from the extracellular fluid and ions constituting apatite crystals are thus possible. It is generally agreed that bone strength depends on the bone matrix volume and the microarchitectural distribution of this volume, while the degree of mineralization of bone tissue is almost never mentioned as a determinant of bone strength. We now have evidence that the degree of mineralization of bone tissue strongly influences not only the mechanical resistance of bones but also the bone mineral density. In adult bone, our model is based on the impact of changes in the bone remodeling rate on the degree of mineralization of bone tissue. The purpose of this paper is to report the main results concerning the interactions of strontium (Sr) with bone mineral in animals and in osteoporotic women treated with strontium ranelate (SR). These studies aimed to evaluate using X-ray microanalysis, X-ray diffraction and computerized quantitative contact microradiography: (1) the relative calcium and Sr bone content, (2) the distribution of Sr in compact and cancellous bone, (3) the dose dependence of the deposition of Sr in bone, (4) the interactions between Sr and mineral at the crystal level (in monkeys), (5) the influence of Sr on the mean degree of mineralization of bone tissue and on the distribution of the degree of mineralization of bone tissue, and (6) the bone clearance of Sr over short periods of time (6 and 10 weeks) after cessation of SR administration (monkeys treated for 13 and 52 weeks, respectively). In monkeys killed at the end of exposure (13 or 52 weeks), Sr was taken up in a dose-dependent manner into compact and cancellous bone, with a higher content in new bone than in old bone. The Sr content greatly decreased (about 2-fold) in animals killed 6 or 10 weeks after the end of treatment but this affected new bone almost exclusively. After SR treatment, there were no significant changes in crystal characteristics. Easily exchangeable in bone mineral, Sr was slightly linked to crystals by ionic substitution (generally 1 calcium ion substituted by 1 Sr ion in each unit cell). The degree of bone mineralization was not significantly different in the various groups of monkeys. Thus, at the end of long-term SR treatment and after a period of withdrawal, Sr was taken up in a dose-dependent manner into new bone without alteration of the degree of bone mineralization and with no major modification of bone mineral at the crystal level. In postmenopausal osteoporotic women treated with SR (0.5, 1 and 2 g/day) for 2 years, Sr was dose-dependently deposited into new bone without changes in the degree of mineralization of bone tissue. These findings could reflect dose-dependent stimulation of bone formation and are of potential value for the use of SR in the treatment of osteoporosis. In conclusion, the different studies performed on bone samples from monkeys and humans treated with various doses of SR showed that Sr was heterogeneously distributed between new and old bone but in a dose-dependent manner without alteration of the crystal characteristics and the degree of mineralization of bone tissue, even after long-term administration of often high doses of SR (the highest therapeutic dose used in humans is 4-fold lower than the lowest experimental dose administered to monkeys). This emphasizes the value, as antiosteoporotic treatment, of SR, which is safe at the bone mineral level.

Animals↗

Determinants of pathological mineralization.

PURPOSE OF REVIEW: Physiological mineralization is necessary for the formation of skeletal tissues and for their appropriate functions during adulthood. Pathological or ectopic mineralization of soft tissues, including articular cartilage and cardiovascular tissues, leads to morbidity and mortality. Recent findings suggest that the mechanisms and factors regulating physiological mineralization may be identical or similar to those regulating ectopic mineralization. Therefore, the purpose of this review is to describe the current knowledge of mechanisms and determinants that regulate physiological mineralization and how these determinants can be used to understand ectopic mineralization better. RECENT FINDINGS: Recent findings have indicated that physiological and pathological mineralization are initiated by matrix vesicles, membrane-enclosed particles released from the plasma membrane of mineralization-competent cells. An understanding of how these vesicles initiate the physiological mineralization process may provide novel therapeutic strategies to prevent ectopic mineralization. In addition, other regulators (activators and inhibitors) of physiological mineralization have been identified and characterized, and evidence indicates that the same factors also contribute to the regulation of ectopic mineralization. Finally, programmed cell death (apoptosis) may be a contributor to physiological mineralization, and if occurring after tissue injury may induce ectopic mineralization and mineralization-related differentiation events in the injured area and surrounding areas. SUMMARY: This review describes how the understanding of mechanisms and factors regulating physiological mineralization can be used to develop new therapeutic strategies to prevent pathological or ectopic mineralization events.

Apoptosis↗

Distribution of mineralization indices of modeling and remodeling over eight months in middiaphyseal cross sections of femurs from adult swine.

BACKGROUND: This study assessed the distribution of active mineral formation sites within the middiaphyseal femoral cross section of swine and determined the extent to which various subsections represented bone formation activity in the entire cross section. METHODS: Twenty adult female swine (sows) were injected with two double (10-day intervals) labels 8 months apart. Labels involved fluorochrome markers of active mineral formation sites. Intact femoral middiaphyseal cross sections were embedded in polymethylmethacrylate, cut, and ground to 80 microm for analysis. Each specimen was subdivided into 16 anatomical and eight geometric subsections. Labeled mineralizing surface and mineral apposition rate were determined in the periosteal and endocortical envelopes. The number of labeled osteons per unit area of bone and osteonal mineral apposition rate were determined in the intracortical envelope. RESULTS: Periosteal mineralizing surface followed a bimodal distribution with highest surface activation on the anterior and posterior segments. Periosteal mineral apposition rate followed a modal distribution with highest apposition rates in the posterior portion of the cross section. The distribution of forming osteons was modal with highest frequencies of labeled osteons in the posterior segment. No significant regional differences were detected for osteonal mineral apposition rate, endocortical mineralizing surface, or endocortical mineral apposition rate. The location of either a single or a combination of two to four subsections that best predicted mineralizing surface and mineral apposition rate in the entire cross section differed with each trait and envelope. Fifty percent of the entire area as alternate anatomical subsections was required to predict > 90% of variation in all traits evaluated. Overall, the predictability of mineralizing surface and mineral apposition rate was similar for geometrically defined subsections. CONCLUSION: At least 50% of the cross-sectional area from alternate anatomical subsections must be measured to predict > 90% of variation in periosteal, intracortical, and endocortical mineralizing surface and mineral apposition rate in the sow middiaphyseal femur.

Animals↗

Variation in bone mineral density of the sacrum in young adults and its significance for sacral fixation.

STUDY DESIGN: Bone mineral density variations throughout the sacrum were measured and correlated with sacral screw insertion torque. OBJECTIVE: To quantify bone mineral density variations within the S1 body and ala of young human specimens, especially along the pathways of sacral screws, and to examine the relation between sacral screw fixation and bone mineral density. SUMMARY OF BACKGROUND DATA: Vertebral bone quality is an essential factor in anterior or posterior screw fixation of the spine. Several studies have been conducted regarding bone mineral density variations in the cervical and thoracolumbar spine. However, such variations in bone mineral density in the sacrum have not been well documented. METHODS: The bone mineral density of 13 sacral specimens from young male cadavers (mean age, 31 years) was measured using highly accurate quantitative computed tomography. Variations in bone mineral density were measured in five transverse layers and seven vertical columns within the S1 body, and in four transverse layers and six vertical columns within the ala. The sacral screw insertion torque was measured (unicortical and bicortical), and the correlation with bone mineral density was calculated. RESULTS: The mean bone mineral density of the S1 body was 381.9 +/- 59 mg/cm3, which was 31.9% higher than that of the sacral ala (mean, 296.9 +/- 86 mg/cm3) (P < 0.05). Bone mineral density of the superior sacral endplate was higher than that of any other transverse layer. Columns near the lateral posterior and lateral anterior of the S1 body had the highest bone mineral density. In the ala, bone mineral density values of the internal columns (pedicle) were the highest. Screw insertion torque for bicortical purchase along the S1 pedicle correlated well with the bone mineral density of the S1 body (r = 0.67, P < 0.05). CONCLUSION: This study quantified the volumetric bone mineral density variations within the S1 body and ala, and a significant linear correlation between the screw insertion torque and bone mineral density was found. Optimal sacral screw insertion pathways were also outlined based on bone mineral density values.

Adult↗

What triggers cell-mediated mineralization?

Mineralization is an essential requirement for normal skeletal development, but under certain pathological conditions organs like articular cartilage and cardiovascular tissue are prone to unwanted mineralization. Recent findings suggest that the mechanisms regulating skeletal mineralization may be similar to those regulating pathological mineralization. In general, three forms of cell-mediated mineralization are recognized in an organism: intramembranous ossification, endochondral ossification and pathological mineralization. This review summarizes recent work that tried to elucidate how cell-mediated mineralization is initiated and regulated. To explain mineralization, several theories have been proposed. One theory proposes that mineralization is initiated within matrix vesicles (MVs). A second, not mutually exclusive, theory proposes that phosphate induces apoptosis, and that apoptotic bodies nucleate crystals composed of calcium and phosphate. A third theory suggests that mineralization is mediated by certain non-collagenous proteins, which associate with the extracellular matrix. Regardless of the way mineralization is initiated, the organism also actively inhibits mineralization by specific proteins and removal of an inhibitor may also induce mineralization. Although many studies greatly contributed to a better understanding of the mechanisms regulating cell-mediated mineralization, many questions remain about the mechanisms that trigger cell-mediated mineralization and how this process is regulated. Further investigation is necessary to develop in the future novel therapeutic strategies to prevent pathological mineralization.

Animals↗

Heritability of bone mineral density.

OBJECTIVE: To evaluate the influence of genetic background as a determinant of peak bone mass. PATIENTS AND METHODS: We compared lumbar spine bone mineral density in 175 girls with a bone age of 16 years or older and in their premenopausal mothers. We also investigated the influence of a family history of osteoporosis on lumbar spine bone mineral density in 275 women and their 559 daughters. RESULTS: In the 175 mother-daughter pairs, heritability (h2) was significantly different from 0 (P < 0.0001) for lumbar spine bone mineral density (h2 = 53%; 95% confidence interval [95% CI] = 28.5-77.6%), bone mineral content (h2 = 62.3%; 95% CI = 37.7-86.8%), bone mineral density adjusted for body mass index (h2 = 56%; CI = 31.5-80.5%), and bone mineral content adjusted for body mass index (h2 = 68.2%; CI = 43.6-92.7%). However, the heritability estimations lacked accuracy, as shown by the wide 95% CIs. Osteopenia and osteoporosis were found in 16.4% and 1% of the mothers, respectively. In the subgroup defined by osteopenia or osteoporosis in the mother, lumbar spine bone mineral density was significantly higher in the daughters than in the mothers (0.994 +/- 0.095 g/cm2 versus 0.895 +/- 0.098 g/cm2; P < 0.0001), whereas the opposite was true in the subgroup defined by normal bone mass in the mothers (1.068 +/- 0.110 g/cm2 versus 1.109 +/- 0.098 g/cm2; P = 0.0003). Nevertheless, lumbar spine bone mineral density was significantly lower in the daughters of low-bone-mass women than in those of normal-bone-mass women (0.994 +/- 0.009 g/cm2 versus 1.069 +/- 0.012 g/cm2; P = 0.0006). These findings suggest a role of genetic factors inherited from the father and also indicate that bone mass gains during adulthood contribute to achievement of the optimal peak bone mass. In the family history study, bone mass was lower in the subjects with a family history of osteoporosis (123 of the 559 daughters, Z-scores normalized for height, weight, and pubertal status: bone mineral density Z-score, -0.054 +/- 1.104; bone mineral content Z-score, -0.014 +/- 1.079; 58 of the 275 mothers: bone mineral density, 1.048 +/- 0.107 g/cm2; bone mineral content, 43.3 +/- 6.8 g) than in those without a family history of osteoporosis (436 daughters, bone mineral density Z-score, 0.006 +/- 0.981; bone mineral content Z-score, -0.007 +/- 0.985; 217 mothers: bone mineral density, 1.070 +/- 0.127 g/cm2; bone mineral content, 43.8 +/- 6.7 g); however, none of these differences were statistically significant. CONCLUSION: Our findings challenge the currently popular concept of marked bone mass heritability but are consistent with early genetic influences on lumbar spine bone mass. Thus, optimization of the peak bone mass acquired during growth may help to prevent osteoporosis.

Adolescent↗

Bone matrix and mineral abnormalities in postmenopausal osteoporosis.

Iliac crest biopsies from 56 postmenopausal osteoporotic females with spontaneous compression fractures and decreased total body Ca were compared to similar tissue from 48 normal controls. Biopsies were analyzed for bone density, Na, Ca, Mg, P, Co3, and hydroxyproline (OH-P). From the results OH-P/matrix, % mineral, and the ion content of the mineral were calculated. osteoporotic subjects showed decreased bone density, % mineral in bone, and OH-P in the bone matrix. Within the mineral, CO3 and Ca/P were decreased, while Na and Mg were increased. Statistical analysis showed that matrix OH-P and % mineral varied independently, and therefore the patients were separated into 4 subgroups: Group Ia: decreased matrix OH-P with normal % mineral (n = 9), Group Ib: decreased matrix OH-P with decreased % mineral (n = 5), Group IIa: normal matrix OH-P with normal % mineral (n = 33), Group IIb: normal matrix OH-P with decreased % mineral (n = 9). Decreased % mineral was associated with decreased bone density and an increase in Na and Mg in the mineral, which suggests skeletal Ca deficiency. Decreased matrix OH-P was associated with decreased bone density and, in the low % mineral group, with decreased mineral CO3 and Ca/P, suggesting a mineral of decreased mean crystal size. When both abnormalities coexisted (Group Ib), the greatest reduction in total body Ca was seen. Patients with normal matrix and normal % mineral (Group IIa) still had decreased bone density. The results suggest that in a large, clinically homogeneous population of postmenopausal osteoporotic women, 4 subgroups can be identified by differences in chemical composition of iliac crest biopsies.

Adult↗

Contribution of mineral waters to dietary calcium and magnesium intake in a French adult population.

OBJECTIVE: To assess the contribution of mineral water containing different amounts of calcium and magnesium to the total dietary intakes of these minerals DESIGN: Matched case control study using data issued from the Supplementation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) cohort. SUBJECTS: Subjects were water consumers-240 men and 424 women-divided into the following 4 groups (n=166 per group): regular drinkers of a calcium-rich and magnesium-rich mineral water (calcium, 486 mg/L; magnesium, 84 mg/ L), drinkers of a water classified as a moderately mineralized content (calcium, 202 mg/L; magnesium, 36 mg/L), drinkers of 2 low-mineralized waters (calcium, 9.9 to 67.6 mg/L and magnesium, 1.6 to 2 mg/L, respectively), and drinkers of tap waters. STATISTICAL ANALYSES: Quantitative data were compared using student's t test. Mean comparisons were performed in multivariate analysis by analysis of variance. RESULTS: Dietary calcium intake provided by the various food groups did not differ between the 4 consumer groups, except for calcium provided by mineral water. According to its calcium concentration, mineral water may contribute to one fourth of the total daily calcium intake. Subjects who regularly drink mineral-rich water have a calcium intake that is significantly higher (P< 10(-3)) than those drinking either low-mineral-content water or tap water. Dietary magnesium intake provided by the various food groups did not differ between the 4 consumer groups, except for magnesium provided by mineral water. Depending on the magnesium concentration of the mineral water, it contributed 6% to 17% of total daily magnesium intake. Drinkers of magnesium-rich mineral water and water with a moderate mineral content had magnesium intakes significantly (P< 10(-3)) higher than those of drinkers on low-mineralized or tap water. APPLICATIONS: Mineral-rich water may provide an important supplementary contribution to total calcium and magnesium intake. For dietetics professionals, it may provide-in place of the usual recommendations concerning the consumption of dairy products-a good way to improve calcium and magnesium intakes, particularly in subjects who don't like dairy products.

Adult↗

The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners.

Limited information is available on the effects of chronic mercury exposure in relation to the risk of cardiovascular disease (CVD). It is known from in vitro and in vivo studies that Hg can promote lipid peroxidation through promotion of free radical generation, and interaction with antioxidative enzymes and reduction of bioavailable selenium. The objective of the study was to test the hypothesis that long-term past occupational exposure to elemental Hg (Hg0) can modify antioxidative capacity and promote lipid peroxidation in miners. The study population comprised 54 mercury miners and 58 workers as the control group. The miners were examined in the post-exposure period. We evaluated their previous exposure to Hg0, the putative appearance of certain nonspecific symptoms and signs of micromercurialism, as well as the main behavioural and biological risk factors for CVD, and determined: 1) Hg and Se levels in blood and urine, 2) antioxidative enzymes, Cu/Zn superoxide dismutase (CuZn-SOD), catalase (CAT), and selenoenzyme glutathione peroxidase (GSH-Px) activity in erythrocytes as indirect indices of free radical activity, 3) pineal hormone melatonin (MEL) in blood and urine, and 4) lipid hydroperoxides (LOOHs) and malondialdehyde (MDA) as lipid peroxidation products. The mercury miners were intermittently exposed to Hg0 for periods of 7 to 31 years. The total number of exposure periods varied from 13 to 119. The cumulative U-Hg peak level varied from 794-11,365 microg/L. The current blood and urine Hg concentrations were practically on the same level in miners and controls. Miners showed some neurotoxic and nephrotoxic sequels of micromercurialism. No significant differences in behavioural and biological risk factors for CVD were found between miners and controls. A weak correlation (r = 0.36, p < 0.01) between systolic blood pressure and average past exposure U-Hg level was found. The mean P-Se in miners (71.4 microg/L) was significantly lower (p < 0.05) than in the controls (77.3 microg/L), while the mean U-Se tended to be higher (p < 0.05) in miners (16.5 microg/g creatinine) than in the controls (14.0 microg/g creatinine). Among antioxidative enzyme activities, only CAT in erythrocytes was significantly higher (p < 0.01) in miners (3.14 MU/g Hb) than in the controls (2.65 MU/g Hb). The mean concentration of B-MEL in miners (44.3 ng/L) was significantly higher (p < 0.01) than in the controls (14.9 ng/L). The mean value of U-MEL sulphate (31.8 microg/L) in miners was significantly lower (p < 0.01) than in the control group (46.9 microg/L). Among the observed lipid peroxidative products, the mean concentration of U-MDA was statistically higher (p < 0.01) in miners (0.21 micromol/mmol creatinine) than in the controls (0.17 micromol/mmol creatinine). In the group of miners with high mercury accumulation and the presence of some nonspecific symptoms and signs of micromercurialism, the results of our study partly support the assumption that long-term occupational exposure to Hg0 enhances the formation of free radicals even several years after termination of occupational exposure. Therefore, long-term occupational exposure to Hg0 could be one of the risk factors for increased lipid peroxidation and increased mortality due to ischaemic heart disease (ICH) found among the mercury miners of the Idrija Mine.

Adult↗

Fungal degradation of calcium-, lead- and silicon-bearing minerals.

The aim of this study was to examine nutritional influence on the ability of selected filamentous fungi to mediate biogenic weathering of the minerals, apatite, galena and obsidian in order to provide further understanding of the roles of fungi as biogeochemical agents, particularly in relation to the cycling of metals and associated elements found in minerals. The impact of three organic acid producing fungi (Aspergillus niger, Serpula himantioides and Trametes versicolor) on apatite, galena and obsidian was examined in the absence and presence of a carbon and energy source (glucose). Manifestation of fungal weathering included corrosion of mineral surfaces, modification of the mineral substrate through transformation into secondary minerals (i.e. crystal formation) and hyphal penetration of the mineral substrate. Physicochemical interactions of fungal metabolites, e.g. H+ and organic acids, with the minerals are thought to be the primary driving forces responsible. All experimental fungi were capable of mineral surface colonization in the absence and presence of glucose but corrosion of the mineral surface and secondary mineral formation were affected by glucose availability. Only S. himantioides and T. versicolor were able to corrode apatite in the absence of glucose but none of the fungi were capable of doing so with the other minerals. In addition, crystal formation with galena was entirely dependent on the availability of glucose. Penetration of the mineral substrates by fungal hyphae occurred but this did not follow any particular pattern. Although the presence of glucose in the media appeared to influence positively the mineral penetrating abilities of the fungi, the results obtained also showed that some geochemical change(s) might occur under nutrient-limited conditions. It was, however, unclear whether the hyphae actively penetrated the minerals or were growing into pre-existing pores or cracks.

Aspergillus niger↗

Determination, by spodography, of the intracellular distribution of mineral matter throughout the life history of Bacillus cereus.

Knaysi, Georges (Cornell University, Ithaca, N. Y.). Determination, by spodography, of the intracellular distribution of mineral matter throughout the life history of Bacillus cereus. J. Bacteriol. 82:556-563. 1961.-The intracellular distribution of mineral matter throughout the life history of Bacillus cereus strain C(3) was investigated by microincineration for which the term spodography is suggested. The organism was grown in microcultures on collodion membranes supported by agar media. At various stages of development, microcultures were floated on distilled water, picked onto cover glasses, air-dried, and incinerated at 500 to 525 C. The mineral residue is deposited in situ and shows the distribution of mineral matter in the cells. Study of the spodograms thus obtained shows that in the spore mineral matter is concentrated in a peripheral layer surrounding a minerally poor core. As soon as the spore begins to germinate, often before one notes any change in its optical properties, the minerally rich layer increases in thickness while the core becomes gradually smaller and finally disappears. The germ cell appears nearly homogeneous, with evidence of mineral aggregation into discrete granules more readily seen in subsequent generations. The nuclei of the vegetative cells are sites of mineral accumulation. In the compound nuclei, minerals seem to be concentrated in a superficial ring around a minerally poor center. In the young forespore, mineral matter is homogeneously distributed. As the spore stage is approached, however, the mineral matter tends to occupy a peripheral position as in the completed spore. The results indicate that the calcium dipicolinate of the spore is principally in the minerally rich, peripheral layer. The relation of this layer to the other peripheral structures of the spore has not been determined. Observation was made with a phase microscope in dark contrast and using a dry objective.

Animals↗