Effective dose conversion factors in paediatric interventional cardiology.

Conversion factors for effective dose (CF(E) = effective dose/dose-area product (mSv (Gy cm2)(-1)) in paediatric interventional cardiology were estimated retrospectively for 249 patients using the dose-area product (DAP), irradiation geometry, exposure parameters and tissue-weighting factors (TWFs) from the International Commission on Radiological Protection (ICRP) 60. Two methods for estimating the conversion factors, which differed in the description of the irradiation geometry, were evaluated. The effective doses obtained with the two methods were almost identical. The results showed that irradiation geometry had no significant impact on the CF(E), and a single factor was defined for both diagnostic and interventional examinations. In addition, the effect of the new tissue-weighting factor for breast tissue (TWF(b)) given in ICRP 103 on the effective dose was assessed. The CF(E) was 3.7+/-0.2 mSv (Gy cm2)(-1) (neonate), 1.9+/-0.2 mSv (Gy cm2)(-1) (1 year), 1.0+/-0.1 mSv (Gy cm2)(-1) (5 years), 0.6+/-0.1 mSv (Gy cm2)(-1) (10 years) and 0.4+/-0.1 mSv (Gy cm2)(-1) (15 years). Applying these CFs to the individual DAP values of each patient yielded mean effective doses of 13.0 mSv (neonate), 8.6 mSv (1 year), 6.4 mSv (5 years), 8.6 mSv (10 years) and 12.7 mSv (15 years). The maximum estimated skin dose (15 patients) did not exceed 60 mGy. With the new ICRP value for TWF(b), increases in the CFs in the order of 10-30%, and in the effective dose of 10-20%, were indicated. The results indicated that the effective dose in paediatric interventional cardiology is of much greater concern than the skin dose. Furthermore, age-dependent CF(E) values are required so as not to underestimate the doses to very young patients.

All-optical control of Bragg grating in semiconductor-coated D-shaped fiber.

A Bragg grating was fabricated in a D-shaped fiber that was subsequently coated with an alpha-Si:H semiconductor film. The reflected spectrum was optically controlled by means of evanescent coupling, shifting to shorter wavelengths with increased control-light power. The effective nonlinearity of the fiber was 2.0 x 10(-10) cm(2)/W . The device was optically tuned by 4.3 x 10(-4) nm/mW , leading to 54% (>3-dB) depth modulation for 230 mW of power.

Neuropeptide Y shifts equilibrium between alpha- and beta-adrenergic tonus in proximal tubule cells.

Renal sympathetic nerves play a central role in the regulation of tubular Na+ reabsorption. Norepinephrine (NE) and neuropeptide Y (NPY) are colocalized in renal sympathetic nerve endings. The purpose of this study is to examine the integrated effects of these neurotransmitters on the regulation of Na+-K+-ATPase, the enzyme responsible for active Na+ reabsorption in renal tubular cells. Studies were performed on proximal tubular segments, which express adrenergic alpha- and beta-receptors, as well as NPY-Y2 receptors. It was found that alpha- and beta-adrenergic agonists had opposing effects on Na+-K+-ATPase activity. beta-Adrenergic agonists induced a dose-dependent inhibition of the Na+-K+-ATPase activity, whereas alpha-adrenergic agonists stimulated the enzyme. NPY abolished beta-agonist-induced deactivation of Na+-K+-ATPase and enhanced alpha-agonist-induced activation of Na+-K+-ATPase. The beta-adrenergic agonist appeared to inhibit Na+-K+-ATPase activity via a cAMP pathway. NPY antagonized beta-agonist-induced accumulation of cAMP. In our preparation, NE alone had no net effect but stimulated the Na+-K+-ATPase activity in the presence of beta-adrenergic antagonists, as well as in the presence of NPY. The results indicate that, in renal tissue, NPY determines the net effect of its colocalized transmitter, NE, by its ability to attenuate the beta- and enhance the alpha-adrenergic effect.

High-reflectivity fiber-optic bandpass filter designed by use of the iterative solution to the Gel'fand-Levitan-Marchenko equations.

A fiber Bragg grating bandpass filter has been investigated. The profile of the 3.1-cm-long grating was synthesized for high reflectivity and low dispersion by use of the iterative solution to the Gel'fand-Levitan-Marchenko equations. A grating designed according to this synthesis was written into a boron-codoped germanosilica fiber. The measured spectral response was in good agreement with simulations. The achieved in-band reflection was 97%, and the passband ripple was only 0.06 dB.

Mutation of the protein kinase C phosphorylation site on rat alpha1 Na+,K+-ATPase alters regulation of intracellular Na+ and pH and influences cell shape and adhesiveness.

The enzyme Na+,K+-ATPase creates the transmembrane Na+ gradient that is of vital importance for functioning of all eukaryotic cells. Na+, K+-ATPase can be phosphorylated by protein kinase A (PKA) and protein kinase C (PKC), and these sites of phosphorylation have been identified. In the present study, we have examined the physiological significance of PKC phosphorylation of rat Na+,K+-ATPase. In COS cells transfected with wild type rat Na+,K+-ATPase alpha1, intracellular Na+ was higher and pH was lower than in cells transfected with rat Na+,K+-ATPase alpha1 in which the PKC phosphorylation site, Ser-23, had been mutated into alanine. Phorbol dibutyrate inhibited Na+,K+-ATPase-dependent ATP hydrolysis and Rb+ uptake in cells expressing wild type Na+,K+-ATPase but not in cells expressing S23A Na+,K+-ATPase. Cells expressing the S23A mutant had a more rounded appearance and attached less well to fibronectin than did untransfected cells or cells transfected with wild type rat Na+, K+-ATPase alpha1. These results indicate a functional role for PKC-mediated phosphorylation of rat Na+,K+-ATPase alpha1 and suggest a connection between this enzyme and cell adhesion.

Position weighting of fiber Bragg gratings for bandpass filtering.

A fiber Bragg grating bandpass filter with tailored refractive-index modulation is investigated. The writing method includes a position weighting technique, which provides flexible and accurate control of the index modulation along the fiber. This weighting is accomplished by adjusting the positions of a large number of overlapping subgratings to control the local grating strength. A 10-cm grating with a truncated sin(x)/x refractive-index modulation function was written and characterized with this method, showing good agreement with simulations. These types of filter are well suited for wavelength-division-multiplexing applications and can be made to have steep edges, low sidelobes, large bandwidth, and low stopband ripple.

Neuropeptide Y regulates rat renal tubular Na,K-ATPase through several signalling pathways.

Neuropeptide Y (NPY) has at least three receptors (Y1, Y2, and Y3) through which it influences different mechanisms in many cell types. Previous data suggest that the Y2 receptor may be divided into prejunctional and postjunctional subgroups. We have examined the intracellular signalling pathways of the postjunctional Y2 receptor in rat renal proximal tubules. The results indicate that NPY regulates Na+,K(+)-ATPase through several signalling pathways: (1) In proximal tubule (PT) cells NPY increased intracellular calcium. The response was blocked by removing extracellular calcium and was also blocked by using nifedipine. This suggests that calcium was increased by influx from the extracellular space through L-type calcium channels. (2) NPY increased Na+,K(+)-ATPase activity in PT segments and this effect was also blocked by nifedipine. CaMKII-Ala286[281-302] a blocker of Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibited the NPY-stimulated Na+,K(+)-ATPase activity. This implies that increased intracellular calcium activates CaMKII which subsequently increases Na+,K(+)-ATPase activity. CaMKII thus appear to act similar to what has been proposed for protein phosphatase 2B. (3) Calphostin C, an inhibitor of protein kinase C (PKC), did not inhibit NPY-stimulated Na+,K(+)-ATPase activity. PKC is, therefore, unlikely to be involved. (4) Y2 receptors are negatively coupled to the cAMP pathway. NPY attenuated forskolin-stimulated cAMP production in renal tubules and exogenous cAMP counteracted the NPY-stimulated Na+,K(+)-ATPase activity. This illustrated the importance of NPY for the regulation of renal sodium handling. We also propose that the renal tubule cell is a good model for studying the function and mechanisms of postjunctional Y2 receptors.

Maturation of rat renal tubular response to alpha-adrenergic agonists and neuropeptide Y: a study on the regulation of Na+,K+-ATPase.

Na+,K+-ATPase in tubular cells plays a pivotal role for the regulation of renal sodium excretion. In adult rats the activity of this enzyme is inhibited by natriuretic hormones and stimulated by antinatriuretic hormones. Here we have examined the tubular response to alpha-adrenergic agonists and neuropeptide Y (NPY) in both infant and adult rats. In the adult kidney, alpha-adrenergic agonists and NPY stimulate Na+,K+-ATPase activity via Ca2+-dependent pathways. Oxymetazoline, a selective alpha-adrenergic agonist, and NPY failed to stimulate proximal tubular (PT) Na+,K+-ATPase activity in 10-d-old rats in doses of 10(-8) to 10(-5) M and 10(-8) to 10(-6) M, respectively, but when tubules were incubated simultaneously with both oxymetazoline 10(-8) M and NPY 5 x 10(-9) M, stimulation was observed in both 10- and 40-d-old rat PT. This effect was abolished by FK 506, an inhibitor of Ca2+ and calmodulin-dependent protein phosphatase 2B in both age groups. A23187, a calcium ionophore, stimulated Na+,K+-ATPase in both infant and adult PT, but 10-fold higher doses were required for the infant tubules. The effect of alpha-adrenergic agonists and NPY on free intracellular Ca2+ was studied in PT cells in primary culture. The Ca2+ response to each agent was less pronounced in infant than in adult cells. Preincubation with NPY, which increases Ca2+ influx into the cells, enhanced the response to the alpha-adrenergic agonist in both infant and adult cells. The results support the concept that the systems regulating renal tubular Na+, K+-ATPase and sodium metabolism undergo postnatal maturation.

C-peptide stimulates rat renal tubular Na+, K(+)-ATPase activity in synergism with neuropeptide Y.

This study was performed in order to test the hypothesis that the connecting peptide of proinsulin, C-peptide, might in itself possess biological activity. Renal tubular Na+, K(+)-ATPase, which is a well-established target for many peptide hormones, was chosen as a model. Rat C-peptide (I) was found to stimulate Na+, K(+)-ATPase activity in single, proximal convoluted tubules dissected from rat kidneys. C-peptide increased the Na+ affinity of the enzyme and all subsequent studies were performed at non-saturating Na+ concentrations. C-peptide stimulation of Na+, K(+)-ATPase activity occurred in a concentration-dependent manner in the dose range 10(-8)-10(-6) mol/l. The presence of neuropeptide Y, 5 x 10(-9) mol/l, enhanced this effect and stimulation of Na+, K(+)-ATPase activity then occurred in the C-peptide dose range 10(-11)-10(-8) mol/l. C-peptide stimulation of Na+, K(+)-ATPase activity was abolished in tubules pretreated with pertussis toxin. It was also abolished in the presence of FK 506, a specific inhibitor of the Ca2(+)-calmodulin-dependent protein phosphatase 2B. These results indicate that C-peptide stimulates Na+, K(+)-ATPase activity, probably by activating a receptor coupled to a pertussis toxin-sensitive G-protein with subsequent activation of Ca2(+)-dependent intracellular signalling pathways.

Regulation of glomerular angiotensin II receptor densities in renovascular hypertension: response to reduced sympathetic and vasopressin influence.

The regulation of the density of angiotensin II receptors in renal glomeruli in response to changes in salt intake is altered in Sprague-Dawley rats with renovascular hypertension due to aortic constriction, and in hypertensive salt-sensitive Dahl rats (Sahlgren 1989, Sahlgren & Aperia 1989). This study examines the modulatory role of sympathetic activity and arginine-vasopressin on angiotensin II receptors in hypertensive Sprague-Dawley rats with aortic constriction as well as in normotensive control rats. Denervation of the left kidney caused a 50% increase in the glomerular angiotensin II receptor density in the denervated kidney in both hypertensive rats and normotensive controls. An even more marked increase in glomerular receptor density occurred in both hypertensive rats and controls after blocking the sympathetic nervous system with guanethidine. To block the effects of arginine-vasopressin we used a blocker of the V1-receptors (predominant in vessels) and found an approximately 100% increase in the glomerular receptor density of angiotensin II in rats with aortic constriction. There was no reduction in blood pressure. Thus, on the receptor level the renin-angiotensin system is markedly influenced by the activity of other major pressor systems.

The benefits of the very early introduction of powdered rice and dried edible seeds (Dal moong) in the oral rehydration solution during the treatment of acute infectious diarrhoea of infancy.

We have examined whether the addition of powdered rice and pulses (Dal moong) to oral rehydration solution will decrease the purging rate and thereby increase the efficacy of the oral rehydration therapy. The study was carried out on 60 male infants, with acute watery diarrhoea, moderate dehydration but without fever, vomiting, or other conditions like septicaemia and meningitis. The infants were treated with either the standard WHO oral rehydration salt solution (ORS) or with a modified solution where glucose was removed and powdered rice and Dal moong were added. We found that the infants receiving ORS with powdered rice and Dal moong had significantly lower fluid losses in the stools, a significant and more rapid weight gain, and needed significantly less fluid than the infants receiving ORS only.

Prolactin, AVP, angiotensin II, corticosterone and aldosterone in the rat during weaning.

In the rat significant changes in the control of body water and electrolyte homeostasis take place during the weaning period (16-24th day of life). This study was performed to analyse how the serum levels of hormones that are known to modulate body water homeostasis change during that period. The serum levels of aldosterone, corticosterone and prolactin increased significantly from 10 to 20 days, whereas those of arginine vasopressin were the same between 10 days and 20 days but increased significantly from 10 to 40 days. Serum levels of angiotensin II increased significantly from 10 to 20 days but decreased from 20 to 40 days, at which time they were significantly lower than in 10-day-old rats. In prolonged-suckling rats, that is, rats which suckled until the 20th day of life, the serum levels of corticosterone, aldosterone and prolactin were somewhat lower than in control rats and those of prolactin were not detectable at 16-20 days. It is concluded that important changes in the serum levels of hormones that regulate body water and electrolyte homeostasis take place during weaning. The postnatal increase in the serum levels of corticosterone and aldosterone is independent of weaning to solid food. The prolactin serum levels seem to be influenced by the length of the nursing period.

Role of arginine-vasopressin for the development of hypertension following aortic constriction.

This study concerns the role of arginine-vasopressin (AVP) for the development of hypertension after constriction of the abdominal aorta proximal to the renal arteries (PAC). The PAC was applied in AVP-deficient Brattleboro (Bb) rats and the blood pressure was recorded 3 weeks later. In untreated rats, PAC did not cause hypertension. When the rats were given AVP 0.6 or 6 nmol day-1 for 2 weeks using mini-pumps, hypertension developed both proximal and distal to the constriction. The level of the hypertension was independent of the AVP dose. When the rats were given I-deamino-4-valine-8-D-arginine-vasopressin (dVDAVP) a specific antidiuretic agonist without effect on the vascular AVP receptors, hypertension did not develop. Sham-operated rats given AVP did not develop hypertension. The PAC rats treated with AVP but not with dVDAVP had an enhanced pressor response to an i.v. bolus dose of angiotensin II. It is concluded that AVP plays an important role in the development of hypertension following aortic constriction and that the action is mediated via the vascular AVP-receptors. We suggest that the presence of AVP permits the expression of other hypertensive factors, such as angiotensin II.

Studies of the renal component of the hypertension in rats with aortic constriction. Role of angiotensin II.

The object of this study was to investigate the renal component of hypertension in aortic constriction. In 40-day-old Sprague-Dawley rats the aorta were constricted either proximal (PAC) or distal (DAC) to the renal arteries. The rats were examined 3 weeks later together with control rats. The arterial pressure proximal to the constriction was elevated in the PAC group but not in the DAC group. In PAC rats the arterial pressure was also elevated distal to the constriction. There was a significant pressure gradient across the constriction in both PAC and DAC rats. The PAC rats had a significant decrease of renal blood flow, a significant increase in renal vascular resistance and a numerical but not significant decrease of glomerular filtration rate. Serum levels of angiotensin II were not significantly different in PAC and control rats. The pressor effect of a bolus dose of angiotensin II was significantly increased in PAC rats. Captopril, a converting enzyme inhibitor, decreased the arterial pressures and renal vascular resistance in PAC rats. The pressure elevating effects of angiotensin II and pressure lowering effect of captopril were more pronounced distal than proximal to the constriction. We conclude that the kidneys play a major role in the development of hypertension in PAC, and that the local effect of angiotensin II on the renal vascular bed is an important contributor to the renal component of the hypertension.