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A high-efficiency, high-power magnicon at 34.272 GHz has been designed and built as a microwave source to develop radio frequency (RF) technology for future multi-TeV electron-positron linear colliders. To develop this technology, this new RF source is being perfected for necessary tests of accelerating structures, RF pulse compressors, RF components, and to determine limits of breakdown and metal fatigue. The design of this high-power amplifier tube, as well as the first experimental results are presented. Index Terms--Accelerating structure, linear collider, magnicon.

Background. The NHE-3 isoform of the Na[sup +]/H[sup +] antiporter, in the apical membrane of renal proximal tubule, is responsible for the bulk transport of Na[sup +] and fluid reabsorption. Studies have reported that apical NHE-3 translocates to internal pools, thereby facilitating natriuresis when blood pressure increases abruptly. Methods. The present study examined Na[sup +]/H[sup +] exchange activity and NHE-3 expression in renal cortical tubules from the spontaneously hypertensive rat (SHR) and WKY rats before and after the development of hypertension. SHR 4 to 6 weeks of age were pre-hypertensive, 6 to 7 weeks old had mild hypertension, and 8 to 13 weeks old had severe hypertension. Renal proximal tubules (PTs) were isolated and purified by Percoll gradient centrifugation. NHE-3 protein and mRNA levels were determined by Western and Northern blots, respectively. Apical brush border membrane vesicles (BBMV) were prepared using the MgSO[sub 4] aggregation method and Na[sup +]/H[sup +] exchange activity assessed using the acridine orange method. Results. Na[sup +]/H[sup +] exchange activity, determined as the rate of Na[sup +]-dependent intracellular pH (pH[sub i]) recovery assessed using BCECF after an acute acid load, was significantly greater in PTs from SHR than in WKY rats at all age groups (4 to 6 weeks, 0.30 ± 0.04 vs. 0.24 ± 0.02 pH U/30 sec, P < 0.05; 6 to 7 weeks, 0.42 ± 0.07 vs. 0.29 ± 0.05 pH U/30 sec, P < 0.05; and 8 to 13 weeks, 0.48 ± 0.07 vs. 0.40 ± 0.07 pH U/30 sec, P < 0.05). The Na[sup +]-dependent recovery in BBMV was also greater in SHR than WKY rats (1464 ± 62 vs. 1042 ± 79 fluorescence. U/5 sec, P < 0.001) and was unaffected by cariporide, a specific NHE-1 inhibitor. NHE-3 protein levels also were significantly higher in SHR than age-matched WKY rats at all stages during the development of hypertension (prehypertensive 1.8-fold; early onset hypertension twofold; established... [ABSTRACT FROM AUTHOR]

Presents information on a study which examined the mechanisms of chlorine transport in rat lymphocytes under a variety of conditions. Methods used; Results; Discussion.

Researchers have frequently correlated estimates of abundance of recruits with oceanographic variables. Our simulation analysis shows that when such correlations are based on estimates of recruits from virtual population analysis (VPA), and when there are time trends in the fishing mortality rate and the oceanographic factor (as is almost always the case, to some degree), the magnitude and statistical significance of correlations depend on the natural mortality rate (M) used in VPA. Our simulation model of an agestructured fish population assumed some correlation between the “true” abundance of recruits and an oceanographic factor, and generated catch data and terminal fishing mortality rates for input to VPA. VPA was then given a set of deliberately mis-specified M values to represent inaccurate knowledge of M; correlations were calculated between the VPA estimates of recruits and the oceanographic factor. When the model's true recruitment was significantly correlated with the oceanographic variable, certain ranges of incorrect M used in VPA resulted in estimated correlations that were not significantly different from zero. When the true correlation was zero, other ranges of incorrect M created spurious correlations between recruitment and the oceanographic factor. First differencing the data used in calculating correlations solved some of the problems but created others. In practice, sensitivity analyses can be used to determine how the choice of M used in VPA influences conclusions about links between the environment and recruitment in fish populations. [ABSTRACT FROM PUBLISHER]

Metabolic alkalosis is a common feature of hypokalemic hypertensive syndromes associated with angiotensin II excess. The alkalosis-generating effect of angiotensin II is usually ascribed to its stimulatory effect on aldosterone secretion, a hormone that upregulates collecting duct hydrogen ion secretion. We studied the effect of angiotensin II infusions on the expression of B1 and a4 protein, subunits of the renal H+-ATPase in adrenalectomized rats. Adrenalectomized rats were given either angiotensin II or vehicle for 7 days via osmotic mini-pumps. H+-ATPase B1 protein expression was evaluated by Western blot analysis in isolated medulla and cortex plasma membrane preparations from one kidney, whereas the contralateral kidney was used for immunostaining. By Western blotting, the relative abundance of B1 protein was 2-fold higher in renal medulla membranes from rats with intact adrenal glands (sham surgery) than from adrenalectomized rats (219+/-47%, n=12; P<0.05). In contrast to renal medulla, adrenalectomy did not significantly alter the relative abundance of B1 protein in renal cortex. Angiotensin II also did not significantly alter the relative levels of B1 protein in the cortex, but it increased it significantly in renal medullary membranes (231+/-56%, n=8; P<0.005). Moreover, enhanced H+-ATPase B1 subunit protein immunoreactivity was found in medullary collecting duct segments of rats infused with angiotensin II. In contrast to B1, expression of a4, another subunit of the H+-ATPase was not altered by adrenalectomy or angiotensin II. We conclude that adrenalectomy decreases whereas angiotensin II increases H+-ATPase B1 subunit expression in medullary, but not in cortical collecting ducts. By increasing the relative abundance of the B1 subunit of H+-ATPase in the collecting duct, angiotensin II excess may lead to increased hydrogen ion secretion and thus metabolic alkalosis-a common feature of hypertensive syndromes associated with angiotensin II overactivity.