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Although microorganisms will preferentially allocate resources to synthesis of nitrogen (N)-acquiring enzymes when soil N availability is low according to the resource allocation model for extracellular enzyme synthesis, a robust link between microbial N-acquiring enzyme activity and soil N concentration has not been reported. To verify this link, we measured several indices of soil N availability and enzyme activity of four N-acquiring enzymes [N-acetyl-ß-glucosaminidase (NAG), protease (PR), urease (UR), and L-asparaginase (LA)] and a carbon (C)-acquiring enzyme [ß-D-glucosidase (BG)] in arable and forest soils. Although the ratios of NAG/BG and PR/BG were not significantly related with indices of soil N availability, ratios of LA/BG and UR/BG were strongly and negatively related with potentially mineralizable N estimated by aerobic incubation but not with pools of labile inorganic N and organic N. These results suggest that microorganisms might allocate their resources to LA and UR synthesis in response to N supply rate rather than the size of the easily available N pools. It was also suggested that the underlying mechanism for synthesis was different between these N-acquiring enzymes in soil microorganisms: microbial LA and UR were primarily synthesized to acquire N, whereas NAG and PR syntheses were regulated not only by N availability but also by other factors.

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The pull-through technique is an interventional radiological procedure used when an occluded lesion cannot be traversed from one direction. To pass the lesion, a long guidewire is traversed from the opposite side and pulled through the ipsilateral sheath using a snare wire. The present report describes a case of severe superior vena cava syndrome treated by stent placement using a pull-through technique with pincer tactics. We successfully placed a stent in the occluded right internal jugular vein to the superior vena cava using a bilateral approach by snaring a guidewire in the right subclavian vein.

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BACKGROUND/AIMS: The L/N-type calcium channel blocker (CCB) cilnidipine has been demonstrated to suppress progressive renal disease in a variety of experimental models, but the characteristic effects of N-type calcium channel blocking action on renal injury have not been examined in detail. Therefore, we investigated the beneficial effects of cilnidipine on renal injury in Dahl salt-sensitive (Dahl S) rats fed a high-sucrose diet (HSD), which mimics metabolic syndrome, and compared them with the effects of an L-type CCB, amlodipine. METHODS: Male Dahl S rats were divided into groups with similar blood pressure at 8 weeks of age and fed an HSD. They received vehicle, cilnidipine or amlodipine for 27 weeks. At 35 weeks of age, urine and blood samples were collected for physiological analysis, and the kidneys were removed for histopathological evaluation. RESULTS: Cilnidipine reduced albuminuria, glomerular hypertrophy, glomerular expression of ICAM-1, ED-1-positive cell infiltration and interstitial fibrosis compared with vehicle-treated rats. In contrast, amlodipine had no effect on these parameters. Urinary norepinephrine excretion, renal expression of renin mRNA and renal tissue levels of angiotensin II were increased only in the amlodipine-treated group. CONCLUSION: Cilnidipine provided superior protection against renal damage compared with amlodipine in Dahl S rats given an HSD. The different effects between these two drugs may be partly explained by their different actions on the renal sympathetic nerve activity and the renin-angiotensin system through the N-type calcium channel blocking action.

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We investigated the relationship between the absorptive pathway and the immune responses of the lung, particularly the phagocytic function of alveolar macrophages (Mphi) after oral administration of D-limonene in rats. D-Limonene was orally administered in oily solution with a stomach tube in thoracic duct-cannulated rats, and the lymphatic output of D-limonene was measured. D-Limonene levels reached a maximum in thoracic duct lymph and lung 3 h after its oral administration. It also significantly increased in bronchoalveolar lavage fluid (BALF) and alveolar Mphi, in which there was frequently a focal exudation of lipid droplets containing D-limonene into the alveolar cavity through alveolar capillary walls. Second, D-limonene orally given to rats (250, 500, 1,000 mg/kg/d) for 8 consecutive days resulted in a marked increase in both the number and the phagocytic activity of alveolar Mphi compared to the controls. BALF from rats dosed with D-limonene (1,000 mg/kg/d) enhanced the phagocytic activity of alveolar Mphi from control rats because the dose was prolonged. The activity of alveolar Mphi following in vitro incubation with D-limonene also increased in a dose-dependent manner. An oral administration of D-limonene enhanced the Con A-stimulated proliferation of splenocytes. These results suggest that D-limonene taken up from the thoracic duct lymph moves to the lung and directly activates the immune response of alveolar MO there, or indirectly activates it through activated lymphocytes.

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The purpose of this study was to investigate the antithrombotic effect and bleeding time prolongation of AJW200, a humanized monoclonal antibody to von Willebrand factor (vWF), in a canine model of coronary arterial thrombosis. AJW200 significantly inhibited cyclic flow reductions, as well as botrocetin-induced platelet aggregation, at 0.1 mg/kg. A significant prolongation of bleeding time was observed at 0.3-1 mg/kg. Approximately 50% occupancy of vWF (approximately 0.7 microg/ml AJW200 in plasma) and 80-100% occupancy (approximately 20 microg/ml AJW200 in plasma) were needed for the antithrombotic effect and the extensive prolongation of bleeding time, respectively. On the contrary, the minimal effective dose of abciximab (0.8 mg/kg) was associated with a significant prolongation of bleeding time. These results suggest that the pharmacological blockade of platelet glycoprotein (GP) Ib-vWF interaction with AJW200 results in a safer antithrombotic profile than platelet GPIIb/IIIa blockade with abciximab in dogs.

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The interaction between platelet glycoprotein Ib and von Willebrand factor (vWF) plays a crucial role in platelet-mediated thrombus formation under high-shear-stress conditions. The aim of this study was to investigate the antiplatelet profile of a humanized anti-vWF monoclonal antibody, AJW200. In vitro studies were performed with a modified cone-and-plate viscometer and human platelets. AJW200 inhibited high-shear-stress-induced platelet adhesion, aggregation, and thrombin generation, but it did not have such effects under low-shear-stress conditions. Although abciximab inhibited platelet aggregation under both shear stress conditions, it did not inhibit platelet adhesion and thrombin generation. In addition, the pharmacokinetics and pharmacodynamics of AJW200 were evaluated in cynomolgus monkeys. Sustained inhibition of ristocetin-induced platelet aggregation was observed over 24 hours, 6 days, and 2 weeks after a single bolus injection of 0.3, 1, and 3 mg/kg, respectively. Moderate prolongation of the bleeding time was observed at the doses of 1 and 3 mg/kg. Abciximab markedly prolonged the bleeding time at 0.4 mg/kg, at which concentration complete inhibition of ADP-induced platelet aggregation was observed. These results suggest that glycoprotein Ib-vWF blockade with AJW200 results in a sustained antiplatelet effect without extensive prolongation of the bleeding time, probably due to a shear-stress-dependent inhibitory action.

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