Clinical value of determining potassium level in erythrocytes of operated-on patients

Since potassium ions are very important in surgical pathology and the course of the postoperative period, the authors determined erythrocyte potassium in 211 patients (37 in the control group and in 174 in the pathological group). The statistically evaluated results were compared for both groups and the correlations of serum and red cell potassium with the acid-base status were studied. The authors used a Marongiu's modified method of potassium determination in a erythrocyte hemolysate with a flame photometer. The mean values for both the control and pathological groups were 84.61 (SD 5.24) and 85.98 (SD 9.10), respectively. The correlation of serum and erythrocyte potassium is subject to many influences and occurs only in the limited pH and HCO3 intervals (pH 7.4 +/- 0.5 and HCO3 21 +/- 2.0) so that it is insignificant even for the control group. If a concentration exceeding two standard deviations is considered abnormal and a deficit percentage is calculated, it is possible to approximate the total body deficit from the expected values of 50-55 mM/kg and to start proper replacement. In evaluating the results, precise laboratory work must be performed and the clinical condition must be taken into account. Therefore, the method of erythrocyte potassium determination is not suitable for routine work and is used only in case of serum potassium excess values and during prolonged postoperative parenteral treatment.     

Aberrometry in the diagnosis of eye diseases

Four methods (by means of Smirnova-Korniushina's aberrometer; with the help of aberroscope--Cherning's lattice; by presenting a figure of a cross; and by automatic refractometry through different portions of the pupil) were used for studying aberration of the optic system of the eye in 490 persons. Among them, 37 were healthy persons, 27--patients with ametropia of moderate degree, 24--with high myopia, 9--with astigmatism above 3.0 D, 16--with monocular diplopia, 327--with keratoconus, 7--with scars of the cornea, 21--with initial cataract, 47--after keratotomy. In norm and in ametropia to 6.0 D, a histogram of refraction distribution by the pupil has a small disperse and a pronounced peak, the Cherning's lattice is straight. In high myopia, the disperse of refraction increases, the peak is slightly pronounced, the lattice is curved along the margins. In astigmatism, the disperse of refraction is great, but there can be peaks. The whole lattice is curved. In monocular diplopia, two more peaks can be seen on the histogram. The lattice is greatly curved. In keratoconus, aberrometry without correction is possible only at the initial stage and shows a rather mixed picture. The histogram of refraction represents a low irregular row. In aberroscopy, the bands are greatly curved, frequently overstep the bounds of the frame that itself looses a form of a circle, becomes oval or polygonal. Contact correction improves the aberration picture considerably. In scars of the cornea, the lattice is distorted and infrequently repeats their forms. In initial cataract, the course of the bands becomes interrupted and rounded spots appear between them.(ABSTRACT TRUNCATED AT 250 WORDS)     

Skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) by inhibiting activation of the IGF-I signaling pathways.

We showed that unloading markedly diminished the effects of IGF-I to activate its signaling pathways, and the disintegrin echistatin showed a similar block in osteoprogenitor cells. Furthermore, unloading decreased alphaVbeta3 integrin expression. These results show that skeletal unloading induces resistance to IGF-I by inhibiting activation of the IGF-I signaling pathways at least in part through downregulation of integrin signaling. INTRODUCTION: We have previously reported that skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) with respect to bone formation. However, the underlying mechanism remains unclear. The aim of this study was to clarify how skeletal unloading induces resistance to the effects of IGF-I administration in vivo and in vitro with respect to bone formation. MATERIALS AND METHODS: We first determined the response of bone to IGF-I administration in vivo during skeletal unloading. We then evaluated the response of osteoprogenitor cells isolated from unloaded bones to IGF-I treatment in vitro with respect to activation of the IGF-I signaling pathways. Finally we examined the potential role of integrins in mediating the responsiveness of osteoprogenitor cells to IGF-I. RESULTS: IGF-I administration in vivo significantly increased proliferation of osteoblasts. Unloading markedly decreased proliferation and blocked the ability of IGF-I to increase proliferation. On a cellular level, IGF-I treatment in vitro stimulated the activation of its receptor, Ras, ERK1/2 (p44/42 MAPK), and Akt in cultured osteoprogenitor cells from normally loaded bones, but these effects were markedly diminished in cells from unloaded bones. These results were not caused by altered phosphatase activity or changes in receptor binding to IGF-I. Inhibition of the Ras/MAPK pathway was more impacted by unloading than that of Akt. The disintegrin echistatin (an antagonist of the alphaVbeta3 integrin) blocked the ability of IGF-I to stimulate its receptor phosphorylation and osteoblast proliferation, similar to that seen in cells from unloaded bone. Furthermore, unloading significantly decreased the mRNA levels both of alphaV and beta3 integrin subunits in osteoprogenitor cells. CONCLUSION: These results indicate that skeletal unloading induces resistance to IGF-I by inhibiting the activation of IGF-I signaling pathways, at least in part, through downregulation of integrin signaling, resulting in decreased proliferation of osteoblasts and their precursors.