Can bone metabolism markers be adopted as an alternative to scintigraphic imaging in monitoring bone metastases from breast cancer?

Bone scintigraphy plays a major role in the diagnosis of bone metastases. The clinical utility of new biochemical markers of bone metabolism has recently been investigated in various bone diseases. This study evaluated the role of some bone metabolism markers in comparison with bone scan in the follow-up of breast cancer patients. We studied 149 patients with breast cancer, 33 (22%) of whom had bone metastases. IRMAs were used for the evaluation of blood levels of osteocalcin, bone alkaline phosphatase (BAP), the C-terminal propeptide of type I procollagen and the C-terminal cross-linked telopeptide of type I collagen (ICTP). Multivariate regression analysis showed that menopausal status (P=0.007) and metastatic bone lesions (P=0.001) affected bone marker levels. When considering post-menopausal women, the only subset in which bone metabolism marker behaviour could be reliably investigated, we found a high degree of overlap in marker distribution for scan-positive and scan-negative patients. Discrimination between scan-negative and scan-positive patients based on the above markers, taken singly or jointly, was assessed by means of logistic discriminant analysis. The best discrimination was achieved with BAP, closely followed by ICTP. BAP and ICTP together gave a slight improvement over the use of the two markers separately. However, even in this case the degree of discrimination was poor and its clinical utility was limited. In fact, to achieve a specificity of 95%, the sensitivity of the test was about 20%; conversely, with a sensitivity of 95%, the specificity was below 10%. In conclusion, based on our findings, we believe that blood levels of the investigated markers cannot replace bone scintigraphy in the follow-up of breast cancer patients for the early detection of bone metastases. Received 14 April and in revised form 5 July 1997     

Effect of prior exercise in Pi/PC ratio and intracellular pH during a standardized exercise. A study on human muscle using [31P]NMR

Seven subjects underwent a standard localized exercise of calf muscles in order to investigate whether the metabolic exercise-induced steady-state, as revealed by the evaluation of inorganic phosphate/phosphocreatine ratio, depends on the conditioning of the muscle just prior to the exercise. The experimental protocols consisted of two separate experiments using first [³¹P]nuclear magnetic resonance spectroscopy and second (on 3 subjects) infrared oxyphotometry to respectively follow variation of energy metabolism and tissular deoxygenation. The exercise consisted of 240 successive plantar flexions (0.5 Hz frequency) against a high load equivalent to SO% of the maximal voluntary contraction. This exercise was accomplished before cold exercise and after warm exercise, a warming-up period bringing to approximately 50% of Vo_2max. The results showed that: (1) steady-state level of phosphate/phosphocreatine and intracellular acidosis was significantly lowered by warming-up; (2) cold and warm exercise steady-state of calculated adenosine diphosphate values were not significantly different; (3) cold exercise rapidly induced a high tissular deoxygenation that is not observed during warm exercise; and (4) time-constant of phosphocreatine resynthesis is lowered after warm exercise but the initial slope of time-evolution is not modified. Parallel experiments also showed that phosphate/phosphocreatine steady-state was not modified in comparison with warm exercise when the same power of exercise was reached by stepwise incrementation of the charge. From these results we postulate that a better tissue oxygenation due to a global or localized warming-up allows to reach the same mechanical performance with a lower decrease of PCr content, owing to a faster adjustment of oxidative metabolism during the transitional period. However the aerobic pathway flux during the steady-state is probably the same before and after the warming-up despite different values of phosphate/phosphocreatine. As a consequence it can be assumed that this ratio is not a good indicator of the rate of muscle oxidative metabolism during the steady-state phase of the exercise.     

成核效应蛋白在泡凝聚融合过程中作用的初步研究

为了探讨成核效应蛋白在泡凝聚、融合过程中的作用，作者研究了胆汁中主要的促成核蛋白系统—ＣｏｎＡ结合蛋白对模拟胆汁泡的形态与脂类组成的影响，发现ＣｏｎＡ结合蛋白在加快泡凝聚与融合的同时，也使泡胆固醇增加，磷脂减少，泡胆固醇／磷脂比增高，认为成核效应蛋白促泡凝聚与融合的本质是改变了泡胆固醇饱和度。作者的初步研究还发现泡相蛋白虽量微却具有强的促成核活性；几种已知的成核效应蛋白在泡相与微胶粒相的分布有差异；胆固醇结石患者与色素结石患者相比，泡蛋白的量与促成核活性均增高。通过泡蛋白亲和染色技术，还发现ＣｏｎＡ结合蛋白能与模拟胆汁泡形成脂质－蛋白复合体。作者认为，泡中成核效应蛋白的存在或量与质的改变，在泡凝聚与融合过程中起重要作用。     

α<Subscript>2β</Subscript> adrenoreceptor 301–303 deletion polymorphism in polycystic ovary syndrome

α_2β adrenoreceptor 301–303 deletion polymorphism does not influence basal metabolic rate, insulin resistance or weight gain in Greek women with polycystic ovary syndrome.     

2型糖尿病并脂肪肝与血脂紊乱的关系探讨

目的　探讨 2型糖尿病并脂肪肝患者与脂代谢紊乱之间的关系。方法　对 60例 2型糖尿病并脂肪肝和 5 2例 2型糖尿病不并有脂肪肝病例的血脂谱 ,空腹血糖 (FPG ) ,餐后 2小时血糖 ( 2hPG) ,空腹胰岛素 (FINS)进行测定 ,计算体重指数 (BMI)及胰岛素敏感指数 (ISI)。结果　 2型糖尿病并脂肪肝与不并脂肪肝相比 ,甘油三脂 (TG) ,低密度脂蛋白胆固醇 (LDL -C) ,FINS均升高 (P <0 .0 5 ,P <0 .0 1) ,而ISI明显降低 (P <0 .0 1)、脂蛋白a(Lp(a)降低(P <0 .0 5 )。结论　 2型糖尿病并脂肪肝比不并脂肪肝者存在明显脂代谢紊乱及胰岛素抵抗     

Thiamine deficiency in utero alters response to ethanol in adulthood

To determine whether prenatal thiamine deficiency, a frequent concomitant of alcoholism, reduces the response to ethanol during adulthood in the rat as does ethanol exposure in utero (Abel et al. 1981), pregnant Sprague-Dawley rats received either control or thiamine deficient diets together with daily injections of the thiamine antagonist pyrithiamine. At 7 months of age, male offspring were exposed to precisely regulated ethanol vapor concentrations in an inhalation chamber for 24 h and blood ethanol concentrations (BECs) and ethanol-induced intoxication were determined. Prenatally thiamine deficient rats and controls were indistinguishable in terms of appearance, body and liver weights, and the ratios of liver to body weight and brain to liver weight. However, total body water was significantly greater, and BECs and behavioral impairment were decreased, in the experimental rats. These findings indicate that prenatal thiamine deprivation is associated with reduced pharmacologic effect of ethanol as a result of increases in its volume of distribution and rate of metabolism.     

A comparison of the effects of a macrobiotic diet and a western diet on drug metabolism and plasma lipids in man

Summary We have compared the effects of two dietary regimens with different macronutrient compositions — a macrobiotic diet and a Western diet — on drug metabolism and plasma lipids in seven healthy volunteers.The macrobiotic diet, high in carbohydrate, low in protein and fat, and devoid of animal food sources, was eaten for a ten day control period, as was the Western diet, high in calories, fat, and protein, as well as animal food sources. We determined the influences of these diets on the clearance of orally administered antipyrine, oxazepam, and methadone, as well as on plasma lipids.There was a statistically significant change in antipyrine clearance as well as in plasma LDL-cholesterol and HDL-cholesterol after the dietary periods. This suggests that the influence of dietary changes may have some effect on the clearance of therapeutic drugs. However, this is not universal and is probably important when the drug is highly dependent on the mixed-function oxidase system.     

胆汁胆固醇对胆囊收缩素受体表达的影响

目的：探讨胆汁胆固醇对胆囊收缩素受体（CCK－R）表达的影响。方法 采用放射免疫分析法和受体放射配基结合法检测对照组、高胆固醇组、自然恢复组及治疗组豚鼠门静脉血CCK水平、胆囊CCK－R的最大结合容量（Bmax）和亲和力（Kd），同时观察空腹胆囊体积（FV）、胆囊胆汁量（FB）和餐后胆囊体积（RV）、胆囊胆汁量（RB）及胆囊收缩率（E％）、胆汁胆固醇浓度的变化。结果 与对照组比较，高胆固醇组豚鼠FV、FB增大（P＜0.05），RV、RB也增大，胆囊收缩率下降（P＜0.01），胆汁胆固醇浓度升高（P＜0.05），门静脉血CCK水平及CCK－R的Kd无改变，而CCK－R的Bmax下降（P＜0.01）；治疗组上述各项指标正常。结论 胆汁中的高胆固醇通过下调胆囊CCK－R表达而导致胆囊收缩功能障碍，降低胆汁高胆固醇浓度可以促进胆囊动力功能的恢复。     

Klinefelter's Syndrome: Hypogonadism,abnormal carbohydrate metabolism. Is it a result of biotin deficiency?

The aetiology of Klinefelter's Syndrome is not known. The causative factor(s) must explain the hypogonadism, low androgen levels, the disordered carbohydrate metabolism and the commonly associated psychiatric conditions. A biotin deficient/dependent state can account for the above. A biotin deficient Klinefelter's Syndrome patients with the above is described. The possible role of biotin in the primary, secondary and tertiary prevention of Klinefelter's Syndrome needs further research.