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While improved crop water‐deficit tolerance is considered of primary importance, many phenotyping efforts focusing on quantifying structural root traits make assumptions about architecture representing root function. Therefore, the aim of this study was to quantify whole plant water‐use traits among disparate peanut (Arachis hypogaea L.) genotypes and determine their impact on water‐deficit tolerance. Mini‐rhizotrons were installed to evaluate genotypic root architecture and developmental changes to two irrigation regimes imposed during early development. Following the early‐season irrigation regimes, above‐ and below‐ground traits were studied across a range of soil water conditions through measures of: (a) leaf‐level gas exchange and (b) soil water depletion quantified using a novel soil water probe inserted into mini‐rhizotrons allowing for matched root architecture and soil water depletion measures. While differential water treatments influenced root system architecture development among the genotypes, soil water depletion locations were primarily determined by water availability in the soil profile, not simply by having greater root length at a given soil location. This contradicts the assumption that greater root presence is a consistent indicator of increased root activity. Phenotypic selection of root traits for improving the efficiency of crop water use should consider both structural and functional traits in relation to the intended production environments slated for future cultivar development. [ABSTRACT FROM AUTHOR]

The role of endothelium-derived hyperpolarizing factor (EDHF) in regulating the pulmonary circulation and the participation of cytochrome P-450 (CYP450) activity and gap junction intercellular communication in EDHF-mediated pulmonary vasodilation are unclear. We tested whether tonic EDHF activity regulated pulmonary vascular tone and examined the mechanism of EDHF-mediated pulmonary vasodilation induced by thapsigargin in salt solution-perfused normotensive and hypoxia-induced hypertensive rat lungs. After blockade of both cyclooxygenase and nitric oxide synthase, inhibition of EDHF with charybdotoxin plus apamin did not affect either normotensive or hypertensive vascular tone or acute hypoxic vasoconstriction but abolished thapsigargin vasodilation in both groups of lungs. The CYP450 inhibitors 7-ethoxyresorufin and sulfaphenazole and the gap junction inhibitor palmitoleic acid, but not 18[alpha]-glycyrrhetinic acid, inhibited thapsigargin vasodilation in normotensive lungs. None of these agents inhibited the vasodilation in hypertensive lungs. Thus tonic EDHF activity does not regulate either normotensive or hypertensive pulmonary vascular tone or acute hypoxic vasoconstriction. Whereas thapsigargin-induced EDHF-mediated vasodilation in normotensive rat lungs involves CYP450 activity and might act through gap junctions, the mechanism of vasodilation is apparently different in hypertensive lungs. pulmonary vasoregulation; pulmonary hypertension; endothelium-derived hyperpolarizing factor; cytochrome P-450; gap junctions; hypoxia

Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme, catalyzing the oxidative cleavage of heme molecules to biliverdin, carbon monoxide, and iron. The present study was designed to investigate the role of HO-1 in the pathogenesis of renal dysfunction during cirrhosis. Biliary cirrhosis was induced in rats by common bile duct ligation (CBDL). Animals were studied 2 and 5 wk after surgery. In kidney from CBDL rats, HO-1 protein expression increased slightly at 2 wk but was abolished at 5 wk. In addition, we confirmed histologically that HO-1 expression was suppressed in renal tubules and interlobular arterioles in 5-wk-old CBDL rats. Conversely, HO-1 expression in liver was strongly increased. Consistent with the development of cirrhosis and renal dysfunction mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal blood flow (RBF) were decreased in CBDL rats compared with sham-operated controls. In sham rats, treatment with the selective HO inhibitor zinc protoporphyrin markedly decreased GFR and RBF to values similar to those measured in CBDL rats without decreasing MAP. In conclusion, decreased renal HO-1 expression contributes to deteriorated renal function and hemodynamics during cirrhosis. This finding provides a novel mechanism for the pathophysiology of renal dysfunction during cirrhosis. endothelial nitric oxide synthase; glomerular filtration rate; renal blood flow; nitric oxide; carbon monoxide

During hepatopulmonary syndrome caused by liver cirrhosis, pulmonary endothelial nitric oxide (NO) synthase (NOS) expression and NO production are increased. Increased NO contributes to the blunted hypoxic pressor response (HPR) during cirrhosis and may induce heme oxygenase-1 (HO-1) expression and carbon monoxide (CO) production, exacerbating the blunted HPR. We hypothesized that NO regulates the expression of HO-1 during cirrhosis, contributing to hepatopulmonary syndrome. Cirrhosis was induced in rats by common bile duct ligation (CBDL). Rats were studied 2 and 5 wk after CBDL or sham surgery. Lung HO-1 expression was elevated 5 wk after CBDL. Liver HO-1 was increased at 2 wk and remained elevated at 5 wk. In catheterized rats, the blunted HPR was partially restored by HO inhibition. Rats treated with the NOS inhibitor [N.sup.G]-nitro-L-arginine methyl ester for the entire 2- or 5-wk duration had normalized HO-1 expression and HPR. These data provide in vivo evidence for the NO-mediated upregulation of HO-1 expression and support the concept that hepatopulmonary syndrome is multifactorial, involving not only NO, but also HO-1 and CO. carbon monoxide; cirrhosis; endothelial nitric oxide synthase; pulmonary vasoreactivity; calcium-activated potassium channels

Research shows that acute hyperoxia in rats modifies sodium pump activity, affecting alveolar sodium resorption and active sodium transport. Experiments designed to assess the effects of hypoxia on lung sodium-potassium-adenosine triphosphatase activity using healthy male Sprague-Dawley rats are described. Isolated, perfused lung preparations are prepared.

The biochemical role of Na-K-adenosine triphosphatase (ATPase) and Na+ pump expression were analyzed in alveolar type II (ATII) cells isolated from the lungs of adult rats after acute exposure to oxygen. Chronic hyperoxic injury in rat ATII cells did not alter normal Na-K-ATPase ion transport. However, hyperoxia-induced acute lung injury decreased maximal enzyme activity and levels of alpha1-subunit antigenic protein.

A surface fluorescence method to quantify transalveolar transport of water, protons and solutes in lungs gives sensitive, time resolved biophysical data from intact organs. The lungs are removed and perfused via the pulmonary artery. The airspace is filled with a solution containing a membrane impermeant fluorescent indicator. Fluorescence signals from the lung surfaces originate from the indicator and provide data on intraalveolar fluid composition. The application of this method shows that the mouse lung has high water permeability which may involve water channels.

Abstract Background We tested the hypothesis that maternal interleukin-1β (IL-1β) pretreatment and induction of fetal cortisol synthesis activates MAP kinases and thereby affects lung fluid absorption in preterm guinea pigs. Methods IL-1β was administered subcutaneously daily to timed-pregnant guinea pigs for three days. Fetuses were obtained by abdominal hysterotomy and instilled with isosmolar 5% albumin into the lungs and lung fluid movement was measured over 1 h by mass balance. MAP kinase expression was measured by western blot. Results Lung fluid absorption was induced at 61 days (D) gestation and stimulated at 68D gestation by IL-1β. Maternal IL-1β pretreatment upregulated ERK and upstream MEK expression at both 61 and 68D gestation, albeit being much more pronounced at 61D gestation. U0126 instillation completely blocked IL-1β-induced lung fluid absorption as well as IL-1β-induced/stimulated ERK expression. Cortisol synthesis inhibition by metyrapone attenuated ERK expression and lung fluid absorption in IL-1β-pretreated fetal lungs. JNK expression after maternal IL-1β pretreatment remained unaffected at either gestation age. Conclusion These data implicate the ERK MAP kinase pathway as being important for IL-1β induction/stimulation of lung fluid absorption in fetal guinea pigs.

In this paper we argue that it is time to adopt a broader classification strategy in forensic and correctional contexts based on the goals associated with offending behaviour. First, we briefly discuss the various roles of classification in science and what constitutes a good classification system. Second, we critically examine current systems of classifying crime and individuals who commit it, concentrating on the use of offense types, levels of risk, and dynamic risk factors. Third, we propose that a forensic/correctional classification system based on functional categories or kinds of behaviour is more likely to result in meaningful descriptive categories, better explanations, and ultimately more effective treatment than our current systems do. We then outline the Functional Offending Behaviour Classification Framework drawing together ideas from evolutionary biology, cognitive neuroscience, psychopathology, disability research, and ethology. Finally, we illustrate the advantages of our functional classification framework in comparison to traditional ways of classifying crime and offending behaviour. [ABSTRACT FROM AUTHOR]

Cadnapaphornchai, Melissa A., Mamiko Ohara, Kenneth G. Morris, Jr., Mladen Knotek, Boris Rogachev, Teri Ladtkow, Ethan P. Carter, and Robert W. Schrier. Chronic NOS inhibition reverses systemic vasodilation and glomerular hyperfiltration in pregnancy. Am J Physiol Renal Physiol 280: F592-F598, 2001.--The chronic role of nitric oxide (NO), independent of prostaglandin synthesis, in the primary peripheral vasodilation, increased glomerular filtration rate (GFR), and renal plasma flow (RPF) in normal pregnancy remains to be defined. The purpose of the present study was to chronically inhibit NOS to return systemic vascular resistance (SVR), cardiac output (CO), GFR, and RPF to nonpregnant values. Pregnant rats received the nitric oxide synthase (NOS) inhibitor, nitro-L-arginine methyl ester (L-NAME), orally from gestational days 7 through 14. Results were compared with nonpregnant and untreated pregnant rats. At 14 days gestation, CO significantly increased in pregnant vs. nonpregnant rats (187 [+ or -] 17 vs. 125 [+ or -] 10 ml/min, P [is less than] 0.05) as SVR decreased (0.64 [+ or -] 0.08 vs. 1.08 [+ or -] 0.08 mmHg [multiplied by] [ml.sup.-1] [multiplied by] min, P [is less than] 0.05) and mean arterial pressure was unchanged (117 [+ or -] 5 vs. 125 [+ or -] 2 mmHg, not significant). Pregnant rats also demonstrated increased GFR (3,015 [+ or -] 33 vs. 2,165 [+ or -] 136 [micro]l/min, P [is less than] 0.01) and RPF (7,869 [+ or -] 967 vs. 5,507 [+ or -] 290 [micro]l/min, P [is less than] 0.05) vs. nonpregnant rats. L-NAME-treated pregnant rats had values for CO (118 [+ or -] 7 ml/min), SVR (1.09 [+ or -] 0.07 mmHg [multiplied by] [ml.sup.-1] [multiplied by] min), GFR (2,264 [+ or -] 150 [micro]l/min), and RPF (5,777 [+ or -] 498 [micro]l/min), which were no different than nonpregnant animals. In summary, similar to human pregnancy, primary peripheral vasodilation occurs early in rat pregnancy. Furthermore, the hyperdynamic circulation and glomerular hyperfiltration of normal rat mid-term pregnancy can be chronically reversed by NOS inhibition. These findings suggest a role for endothelial damage and decreased NO in the pathogenesis of preeclampsia. peripheral arterial vasodilation; normal pregnancy; nitric oxide synthase

Xu, Lieming, Ethan P. Carter, Mamiko Ohara, Pierre-Yves Martin, Boris Rogachev, Kenneth Morris, Melissa Cadnapaphornchai, Mladen Knotek, and Robert W. Schrier. Neuronal nitric oxide synthase and systemic vasodilation in rats with cirrhosis. Am J Physiol Renal Physiol 279: F1110-F1115, 2000.--Cirrhosis is typically associated with a hyperdynamic circulation consisting of low blood pressure, low systemic vascular resistance (SVR), and high cardiac output. We have recently reported that nonspecific inhibition of nitric oxide synthase (NOS) with nitro-L-arginine methyl ester reverses the hyperdynamic circulation in rats with advanced liver cirrhosis induced by carbon tetrachloride (C[Cl.sub.4]). Although an important role for endothelial NOS (eNOS) is documented in cirrhosis, the role of neuronal NOS (nNOS) has not been investigated. The present study was carried out to specifically investigate the role of nNOS during liver cirrhosis. Specifically, physiological, biochemical, and molecular approaches were employed to evaluate the contribution of nNOS to the cirrhosis-related hyperdynamic circulation in C[Cl.sub.4]-induced cirrhotic rats with ascites. Cirrhotic animals had a significant increase in water and sodium retention. In the aorta from cirrhotic animals, both nNOS protein expression and cGMP concentration were significantly elevated compared with control. Treatment of cirrhotic rats for 7 days with the specific nNOS inhibitor 7-nitroindazole (7-NI) normalized the low SVR and mean arterial pressure, elevated cardiac index, and reversed the positive sodium balance. Increased plasma arginine vasopressin concentrations in the cirrhotic animals were also repressed with 7-NI in association with diminished water retention. The circulatory changes were associated with a reduction in aortic nNOS expression and cGMP. However, 7-NI treatment did not restore renal function in cirrhotic rats (creatinine clearance: 0.76 [+ or -] 0.03 ml [multiplied by] [min.sup.-1] [multiplied by] 100 g body [wt.sup.-1] in cirrhotic rats vs. 0.79 [+ or -] 0.05 ml [multiplied by] [min.sup.-1] 100 g body [wt.sup.-1] in cirrhotic rats+7-NI; P NS.). Taken together, these results indicate that nNOS-derived NO contributes to the development of the hyperdynamic circulation and fluid retention in cirrhosis. nitric oxide; liver disease; systemic hemodynamics

Carter, Ethan P., Koichi Sato, Yoshiteru Morio, and Ivan F. McMurtry. Inhibition of [K.sub.Ca] channels restores blunted hypoxic pulmonary vasoconstriction in rats with cirrhosis. Am J Physiol Lung Cell Mol Physiol 279: L903-L910, 2000.--Rats with liver cirrhosis exhibit the hepatopulmonary syndrome composed of blunted hypoxic pulmonary vasoconstriction and arterial hypoxemia. The purpose of this study was to investigate the roles of nitric oxide (NO) and endothelin-1 (ET-1) in the blunted hypoxic pressor response (HPR) in rats with common bile duct ligation (CBDL). Lungs from CBDL rats exhibited markedly blunted HPR, increased endothelial NO synthase (NOS) protein expression, and decreased ET-1 mRNA and peptide expression. The blunted HPR was not reversed by sequential NOS and soluble guanylyl cyclase inhibition by nitro-L-arginine and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ), respectively, or by NOS inhibition combined with ET-1 addition. The blunted HPR was not due to a generalized inability to vasoconstrict because perfusion pressure was equally elevated by increased perfusate KCl in CBDL and sham lungs. After KCl vasoconstriction, HPR was potentiated and did not differ between CBDL and sham lungs. Blunted HPR was also completely restored in CBDL lungs treated with nitro-L-arginine, ODQ, and the [Ca.sup.2+]-activated [K.sup.+] channel blockers apamin and charybdotoxin. These results indicate that although CBDL-induced liver cirrhosis is associated with increased NO and decreased ET-1 in the lung, the blunted HPR is a result of additional factors and appears to involve [Ca.sup.2+]-activated [K.sup.+] channel activation. pulmonary circulation; liver cirrhosis; nitric oxide; calcium-activated potassium channel; endothelin-1