Hypophosphataemia and Hyperphosphataemia in a Hospital Population

One hundred cases of hypophosphataemia (≤ 2·0 mg/100 ml) and 84 cases of hyperphosphataemia (≥ 5·0 mg/100 ml) occurring in a hospital population were studied in order to determine the cause of the abnormality. Examples of hyperphosphataemia due to renal failure were excluded from the study.A low serum phosphorus concentration was most frequently due to intravenous administration of carbohydrate, usually glucose, which accounted for 40% of cases. The next commonest cause was vomiting (12%). No obvious explanation could be found in 26% of cases, but in most of these factors were present which are known to affect phosphorus metabolism.No one cause of hyperphosphataemia was outstanding in frequency and in over 50% of cases no definite explanation for the abnormality could be found.     

Oral Calcium-loading Test in Infancy,with Particular Reference to Idiopathic Hypercalcaemia

An oral calcium-loading test suitable for infants is described and the usual response defined. In four acute cases of idiopathic hypercalcaemia a high and sustained rise in serum calcium occurred, suggestive of hyperabsorption and consistent with a vitamin-D-like effect. In four further infants with a milder illness suggestive of hypercalcaemia the fasting calcium levels were not grossly raised, but the test produced an exaggerated hypercalcaemic response. In this type of patient the test is more sensitive in the diagnosis of idiopathic hypercalcaemia than isolated measurements of serum calcium, especially if these are taken in the fasting state. Five patients on treatment and three whose treatment had been discontinued (but who subsequently relapsed or made a poor recovery) showed abnormal loading tests at a time when fasting calcium levels were normal. In two cases full recovery from the disease was associated with reversion of the test to normal. The test can therefore be used to indicate activity of the disease and consequently as a guide to therapy. In two cases a persistently abnormal loading test was associated with a poor long-term prognosis.     

Defective Intestinal Phosphate Absorption in Familial and Non-familial Hypophosphataemia

With an oral phosphate tolerance test a primary defect in intestinal phosphate absorption was found in patients with untreated familial and non-familial hypophosphataemia. It is suggested that this plays a major part in the aetiology of rickets and osteomalacia in these disorders. Vitamin D was shown to have a beneficial effect on intestinal transport of phosphate, though defective absorption was not completely corrected. If intestinal phosphate absorption is normal, oral phosphate supplements will maintain normal plasma phosphate levels even in the presence of a pronounced renal phosphate leak.In familial and non-familial hypophosphataemia the phosphate tolerance test may be a more sensitive index of genetic abnormality than a low plasma phosphate. It may be helpful in distinguishing several syndromes at present classified under non-familial hypophosphataemia, as well as assessing the response to treatment with vitamin D and in investigating intestinal transport of phosphate.     

肥大细胞释放生物活性介质促进TNCB致敏淋巴细胞分泌IL-17

氯化苦咪酸(TNCB)是诱导接触性超敏反应(CHS)实验模型的常用试剂,IL-17参与CHS的致病过程。利用TNCB致敏C57BL/6小鼠,4d后无菌分离淋巴结细胞。同时制备并体外活化同源小鼠成熟骨髓来源的肥大细胞(BMMC),成熟的BMMC具有肥大细胞特异性表型(FcεRI+/c-kit+),活化后可分泌TNF-α和IL-6等生物活性介质。在抗原提呈细胞存在下,活化的BMMC与淋巴结细胞体外共同培养72h,结果显示,与未致敏淋巴细胞共同培养组相比,BMMC与TNCB致敏淋巴细胞的共同培养上清中IL-17分泌水平显著增高(P0.01)。由此提示,活化的肥大细胞通过释放生物活性介质,促进TNCB致敏淋巴细胞IL-17的分泌。     

Inability to detect organo-silicon compounds in Equisetum and Thuja

Silicon in Equisetum arvense sap has low molar mass and is probably monomeric silicic acid. Tris(β-thujaplicine)silicon X complexes (X  Cl, I₃) were synthesized but could not be found in extracts of Thuja plicata.     

Chloride Transport in Chara corallina and the Electrochemical Potential Difference for Hydrogen Ions

The pH of the cytoplasm of Chara corallina cells has been measuredwith the weak acid 5,5-dimethyloxazolidine-2,4-dione (DM0).Over an external pH range 4·5–9·5 the resultsfit the regression equation pH_cytoplasm=6·28+0·22pH_out. Using measured values of the electric potential difference acrossthe plasmalemma we have calculated the electrochemical potentialdifference across this membrane for H⁺ and Cl^–. Thesedata are used to test the hypothesis that the inward transportof Cl^– is coupled to the inthix of H⁺ or, which comesto the same thing, efflux of OH^–. One-for-one couplingwill not give net Cl^– uptake from solutions with pH greaterthan about 7·2, unless the cytoplasmic Cl^– concentrationis lower than 10 mM, or the pH just outside the membrane islower than that in the bulk solution. It is shown that net Cl^–uptake proceeds from solutions with pH up to 9. The alternative possibility is that Cl^– transport is broughtabout by co-transport of two H⁺ for each Cl^–; this isnot ruled out by the results reported. Such a mechanism mightbe detectable by its electrogenic effect: although such effectshave not been detected, it is shown that they would be smallunder most conditions. Other possible mechanisms are discussed.