The effect of fluoride treatment on bone mineral crystals in the rat

In order to investigate the effect of fluoride on bone mineral crystals, we gave groups of female rats 8 mM NaF/L water and distilled water to control groups. The rats were sacrificed at six weeks, three months, and six months. The fluor content of the bone was determined by neutron activation. X-ray diffraction showed no difference in bone crystal size/ strain with fluoride treatment. Fourier transform Infrared Spectroscopy (FTIR) showed an increased crystallinity in fluoride-fed animals, which seems to be associated with a decrease of labile phosphate environment. Three carbonate bands have been found in fluoridated and normal bone samples. The distribution of carbonate ions on type A and B sites is strongly affected by fluoride. Type A carbonate is always present in bone, but decreases with increasing bone fluoride content. A carbonate band found at 866 cm⁻¹ may correspond to a fluoride interaction with type B carbonate ions. Lastly, phosphate bands have been found to be shifted towards high wave number, which is probably related to the change in unit cell size induced by the fluoride ion. AH these changes induced by fluoride reduce the solubility of bone crystals by direct incorporation of fluoride ions in the apatite lattice and by decreasing the labile phosphate environments.     

The discrepancy in the carbonate found in fish bone and blood

It has been reported in the literature that fish, to get sufficient oxygen, must overventilate with respect to CO₂ and therefore exhibit a low circulating level of bicarbonate.Accordingly, the bones of trout and carp were analyzed to learn if the composition of their bone mineral reflects the low serum level of bicarbonate. It was found that the CO₂ content of fish bone is not significantly different from that of normal mammalian bone.Synthetic apatite crystals, made under comparable conditions of T, , and (HCO ₃ ^– ) were found to contain only 1/7th to 1/8th the CO₂ of fish bone.These data strongly suggest that the composition of the fluids in bone does not reflect, in a simple way, the composition of the circulating serum as is generally assumed.This work was supported in part by the United States Public Health Service Training Grant No. 1 T1 DE 175-02 and in part by the United States Atomic Energy Commission Contract No. W-7401-Eng-49 and has been assigned Report No. UR-49-922.     

含碳酸盐氟羟磷灰石新型抛光膏的研制

目的:用含碳酸盐氟羟磷灰石(FCHA)抛光膏对离体牙牙面进行抛光效果观察.方法:采用FCHA粉料调制抛光膏,用显微硬度计测定材料的显微硬度,并利用电镜观察颗粒形貌和抛光效果.结果:600℃煅烧的FCHA显微硬度为460 N/mm2,颗粒小于76 μm,边角圆钝,适宜作抛光剂.结论:FCHA抛光膏有明显的抛光作用而且还具有脱敏作用,是一种极佳的抛光剂.     

A dicarboxylate/4-hydroxybutyrate autotrophic carbon assimilation cycle in the hyperthermophilic Archaeum Ignicoccus hospitalis

Ignicoccus hospitalis is an anaerobic, autotrophic, hyperthermophilic Archaeum that serves as a host for the symbiotic/parasitic Archaeum Nanoarchaeum equitans. It uses a yet unsolved autotrophic CO(2) fixation pathway that starts from acetyl-CoA (CoA), which is reductively carboxylated to pyruvate. Pyruvate is converted to phosphoenol-pyruvate (PEP), from which glucogenesis as well as oxaloacetate formation branch off. Here, we present the complete metabolic cycle by which the primary CO(2) acceptor molecule acetyl-CoA is regenerated. Oxaloacetate is reduced to succinyl-CoA by an incomplete reductive citric acid cycle lacking 2-oxoglutarate dehydrogenase or synthase. Succinyl-CoA is reduced to 4-hydroxybutyrate, which is then activated to the CoA thioester. By using the radical enzyme 4-hydroxybutyryl-CoA dehydratase, 4-hydroxybutyryl-CoA is dehydrated to crotonyl-CoA. Finally, beta-oxidation of crotonyl-CoA leads to two molecules of acetyl-CoA. Thus, the cyclic pathway forms an extra molecule of acetyl-CoA, with pyruvate synthase and PEP carboxylase as the carboxylating enzymes. The proposal is based on in vitro transformation of 4-hydroxybutyrate, detection of all enzyme activities, and in vivo-labeling experiments using [1-(14)C]4-hydroxybutyrate, [1,4-(13)C(2)], [U-(13)C(4)]succinate, or [1-(13)C]pyruvate as tracers. The pathway is termed the dicarboxylate/4-hydroxybutyrate cycle. It combines anaerobic metabolic modules to a straightforward and efficient CO(2) fixation mechanism.     

碳酸锂合并喹硫平治疗双相障碍抑郁发作的疗效和安全性研究

目的探讨碳酸锂合并喹硫平对双相障碍抑郁发作患者的疗效和安全性。方法共入组67例双相障碍患者接受为期8周的开放性治疗,将所有入组患者随机分为两组,研究组（37例）采用碳酸锂合并喹硫平治疗,对照组（30例）单用碳酸锂,在基线期,第1、2、4、8周末采用汉密顿抑郁量表（hamilton depression scale,HAMD-17）评定疗效,采用治疗副反应量表（treatment emergent symptom scale,TESS）评定不良反应。结果基线期两组HAMD-17评分差异无统计学意义（P〉0.05）,研究组和对照组各完成研究31例和25例。在治疗后第2、4周研究组比对照组HAMD-17评分下降更明显,差异均有高度统计学意义（均P〈0.01）,在治疗第8周后研究组与对照组HAMD-17评分比较差异无统计学意义（P〉0.05）。两组主要不良反应比较差异无统计学意义（P〉0.05）。结论碳酸锂合并喹硫平较单用碳酸锂治疗双相障碍抑郁发作起效更快,不良反应相当,最终总体疗效相当。     

Calcium Carbonate Precipitation in Bicarbonate Hemodialysis

Calcium carbonate has been observed to precipitate in the fluid pathway of dialysate delivery systems dispensing bicarbonate-containing dialysates. Such precipitation can occlude the fluid pathway, leading to system malfunction and increased maintenance requirements. We show that commercial supplies of sodium bicarbonate are contaminated by trace amounts of sodium carbonate. This contamination may result in immediate precipitation of calcium carbonate on formulation of the dialysate, since bicarbonate-containing dialysates, as formulated, are metastable with respect to calcium carbonate. Sparging of the bicarbonate-containing concentrate with carbon dioxide converts any carbonate to bicarbonate, thus avoiding the formation of precipitates on addition of calcium ions.     

Organic and inorganic forms of selenium inhibited differently fish (Rhamdia quelen) and rat (Rattus norvergicus albinus) delta-aminolevulinate dehydratase

Selenium contamination in the aquatic environment can produce severe toxic effects to fish. The mammalian sulfhydryl-containing enzyme, delta-aminolevulinate dehydratase (delta-ALA-D), is inhibited after exposure to organic and inorganic forms of selenium. In the present study, the inhibitory effect of (PhSe)2, (BuSe)2, and Na2SeO3 on the activity of fish hepatic and gill delta-ALA-D was investigated and compared with the rat liver enzyme. Results indicated that delta-ALA-D activity varied considerably depending on the tissue, selenium form, and species considered. For fish (liver and gill), the IC50 values for delta-ALA-D inhibition by (PhSe)2, (BuSe)2, and Na2SeO3 were 274 and 76, 985 and 693, and 386 and 902 microM, respectively. For rat liver these values were 7, 10, and 5 microM, respectively. In contrast, fish and rat subcellular fractions similarly increased the oxidative effect of (PhSe)2 toward sulfhydryl groups from DTT. These catalytic properties of subcellular fractions from fish and rat liver were abolished by heat treatment. Taking into account that aquatic organisms can be in contact with higher concentrations of selenium for longer periods of time and accumulate more selenium than terrestrial animals, it is reasonable to suppose that fish delta-ALA-D can be a potential target for organic and inorganic selenium forms present in aquatic contaminated environments. From an ecotoxicological point of view, our results suggest a link between selenium-induced anemia signs in fish and the sensitivity of fish delta-ALA-D to selenium in natural habitats.     

Heme requirement and acquisition by extracellular and intracellular stages of Leishmania mexicana amazonensis

The inability to synthesize heme, a well known metabolic defect of trypanosomatid protozoa, accounts for their growth requirement for heme compounds in vitro. We now extend this finding to a pathogen Leishmania mexicana amazonensis, especially the intracellular replicative stage of amastigotes in the macrophage. We measured the level of heme and its biosynthetic enzymes, aminolevulinate dehydratase and porphobilinogen deaminase in the parasites and in infected and non-infected macrophages of J774G8 line. Succinylacetone was used to inhibit heme biosynthesis. Leishmanias transform and grow only in medium containing either heme (usually supplied as hemin) or protoporphyrin IX (the latter is leishmanicidal at high concentrations). We detected 1.2, 8.5 and 25 pmol mg-1 protein of heme in amastigotes, promastigotes and macrophages, respectively. The activities of porphobilinogen deaminase and aminolevulinate dehydratase in macrophages were 70 and 2400 pmol h-1 mg-1 protein, respectively. Leishmania-infected macrophages gave the same results and leishmanias had negligible activities of these enzymes. Succinylacetone at 10(-9)-10(-3) M had no effect on leishmanias, but dose-dependently inhibited the activity of aminolevulinate dehydratase to a negligible level and lowered that of porphobilinogen deaminase in macrophages, resulting in a maximum of 66% reduction in intracellular heme. Amastigotes grew equally well in succinylacetone-treated and control untreated macrophages. The results suggest that L. m. amazonensis, incapable of heme biosynthesis, acquires heme exogenously from the culture medium, i.e., fetal bovine serum, independent of the heme synthesized by the macrophages.     

碳酸锂合并氯氮平治疗躁狂症20例临床分析

为观察碳酸锂和氯氮平联合对躁狂症的治疗效果,将20例双相情感性精神障碍躁狂相或躁狂发作的病人应用碳酸锂和氯氮平进行治疗,并应用躁狂量表进行评定。结果发现,治疗6周后,20例病人的躁狂症状有显著性的降低(P<0.01),总有效率为100％。但是这种联合的治疗方法也有不少副作用,其中以便秘、头昏头晕、嗜睡、流涎比较多见。提示:氯氮平与碳酸锂联合治疗躁狂症有显著效果,但需要注意副反应的预防和治疗。     

以纸片法筛查儿童铅毒性易感性的方法学研究

目的：建立以纸片末梢血筛查儿童铅毒性易感性的方法。方法：以Chelex 100 为介质及氯仿法抽提基因组DNA,并比较二者的DNA得率。PCR扩增σ-aminolevulinate dehydratase(ALAD)基因片段,以限制性内切酶MspⅠ分析ALAD基因型。结果：以Chelex 100 为介质抽提基因组DNA的得率为 17.1 μg/ml,氯仿法抽提基因组DNA的得率为 17.5 μg/ml,两种之间的差异无显著性意义(P>0.05)。以两种方法提取的DNA为模板扩增ALAD基因片段及进行ALAD基因型分析均具有较高的特异性,但以Chelex 100 为介质抽提基因组DNA扩增时敏感性有所降低。结论：以纸片末梢血分析ALAD基因型的方法来筛查儿童铅毒性作用的易感人群在技术上是可行的。