A method for evaluating root-knot nematode infection in rice using a transparent paper pouch.

The root-knot nematode (RKN) Meloidogyne incognita is one of the most economically damaging plant-parasitic nematodes. Molecular studies of the plant-RKN interaction have been vigorously carried out in dicotyledonous model plants, while the host range of M. incognita is wide including monocotyledonous plants. As M. incognita causes quality and yield losses in rice (Oryza sativa L.) cultivated in both upland and irrigated systems, we developed a method to examine the plant-RKN interaction in this model monocotyledonous crop plant. Here, we show that a transparent paper pouch could be used to evaluate nematode infection rates in rice with similar results to that of the traditional soil method. The system using a transparent paper pouch can be used to observe the spatial and temporal distribution of developing galls and can save the space of growth chamber.

Water-immersion restraint stress disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats.

We examined whether water-immersion restraint stress (WIRS) disrupts nonenzymatic antioxidant defense systems through ascorbic acid depletion in the adrenal gland of rats. Rats were exposed to WIRS for 0.5, 1.5, 3 or 6 h. WIRS increased serum adrenocorticotropic hormone, corticosterone and glucose concentrations and adrenal corticosterone content at each time point. WIRS increased adrenal lipid peroxide content at 3 and 6 h, and the increase was twofold higher than the unstressed level at 6 h. WIRS decreased adrenal ascorbic acid content at each time point, and the decrease reached one-third of the unstressed level at 6 h. WIRS increased adrenal reduced glutathione content at 0.5 and 6 h but reduced that content to half of the unstressed level at 6 h. WIRS increased adrenal α-tocopherol content at 1.5 h but returned that content to the unstressed level thereafter. When rats with 6 h of WIRS was orally preadministered with l-ascorbic acid (250 mg/kg), WIRS-induced changes in adrenal lipid peroxide, ascorbic acid and reduced glutathione contents were attenuated without any change in stress response. These results indicate that WIRS disrupts nonenzymatic antioxidant defense systems through rapid and continuous ascorbic acid depletion in the adrenal gland of rats.

Giant coronary artery aneurysm with coronary arteriovenous fistula draining into the coronary sinus.

A 77-year-old patient suffering from a giant right coronary artery aneurysm with coronary arteriovenous fistula was admitted to our hospital. The fistula could not be documented preoperatively by computed tomography or coronary angiography but was documented intraoperatively by transesophageal echocardiography (TEE). However, TEE was unable to visualize the draining site of the fistula. Direct palpation by the surgeon ultimately confirmed that the fistula was draining into the coronary sinus. The fistula was closed and the volume of the aneurysm reduced by partial resection. The postoperative course of the patient was uneventful. Giant aneurysms occasionally displace cardiac structures. In such cases, combined imaging technologies, including TEE, may be needed for precise assessment of the giant aneurysm and fistula.

Protective effect of L-ascorbic acid against oxidative damage in the liver of rats with water-immersion restraint stress.

We examined whether L-ascorbic acid (AA) (or reduced ascorbic acid) protects against oxidative damage in the liver of rats subjected to water-immersion stress (WIRS). AA (100, 250 or 500 mg/kg) was orally administered at 0.5 h before the onset of WIRS. Rats with 6 h of WIRS had increased serum corticosterone, glucose, total ascorbic acid (T-AA), AA, lipid peroxide (LPO), and NOx concentrations and alanine aminotransferase and aspartate aminotrasferase activities. The stressed rats had increased hepatic LPO, NOx, and dehydroascorbic acid concentrations and myeloperoxidase activity, decreased hepatic T-AA, AA, reduced glutathione concentrations and superoxide dismutase activity, and unchanged hepatic vitamin E concentration. Pre-administered AA attenuated the stress-induced changes in serum LPO and NOx concentrations and alanine aminotransferase and aspartate aminotrasferase activities and hepatic LPO, NOx, and T-AA, AA, dehydroascorbic acid, and reduced glutathione concentrations and myeloperoxidase and superoxide dismutase activities dose-dependently. Pre-administered AA did not affect the stress-induced changes in serum corticosterone and glucose concentrations. These results indicate that pre-administered AA protects against oxidative damage in the liver of rats with WIRS possibly by attenuating disruption of the antioxidant defense system and increases in NO generation and neutrophil infiltration in the tissue.

Vitamin E protects against stress-induced gastric mucosal lesions in rats more effectively than vitamin C.

In this study, we examined the protective effects of vitamin E (VE) against gastric mucosal lesions induced by water immersion restraint stress (WIRS) in rats in comparison with that of vitamin C (VC). The gastric mucosa of rats with 6 h of WIRS showed lesions with bleeding, decrease in nonprotein SH, VC, VE, and adherent mucus concentrations and constitutive nitric oxide synthase activity, and increase in lipid peroxide and NOx (nitrite/nitrate) concentrations and myeloperoxidase, xanthine oxidase, and inducible nitric oxide synthase activities. Either VE (0.05 or 0.5 mmol/kg) or VC (0.5 or 1.5 mmol/kg) was orally administered to rats with 6 h of WIRS just before the onset of the stress. Both doses of pre-administered VE prevented gastric mucosal lesion development and attenuated all these changes in gastric mucosal components and enzymes studied, whereas only the higher dose of pre-administered VC suppressed the changes in all parameters studied. These results indicate that orally administered VE protects against WIRS-induced gastric mucosal lesions in rats more effectively than orally administered VC. These results also suggest that the administered VE protects against gastric mucosal lesions in rats with WIRS through its antioxidant and anti-inflammatory actions in the gastric mucosa in the same way as the administered VC.

Compound 48/80 causes oxidative stress in the adrenal gland of rats through mast cell degranulation.

Rats were intraperitoneally treated once with compound 48/80 (C48/80), a mast cell degranulator, (0.75 mg/kg). Serum serotonin, histamine and corticosterone levels increased 0.5 h after C48/80 treatment, but their increases were reduced thereafter. Adrenal total ascorbic acid (ascorbic acid plus dehydroascorbic acid), ascorbic acid and dehydroascorbic acid levels decreased 0.5, 3 or 6 h after C48/80 treatment, adrenal lipid peroxide level increased at 3 and 6 h, adrenal non-protein-SH level decreased at 3 and 6 h and adrenal beta-tocopherol level decreased at 3 h. Ketotifen, a mast cell stabilizer (1 mg/kg) administered intraperitoneally at 0.5 h before C48/80 treatment, attenuated all these changes found in the serum and adrenal at 3 h after treatment, while beta-tocopherol (250 mg/kg), administered orally at 0.5 h after C48/80 treatment, attenuated all these changes in the adrenal tissue. These results indicate that C48/80 causes oxidative stress in rat adrenal gland through mast cell degranulation.

Involvement of oxidative stress in increases in the serum levels of various enzymes and components in rats with water-immersion restraint stress.

The plasma or serum levels of various enzymes and components are known to increase in rats with water-immersion restraint stress (WIRS). We examined whether oxidative stress is involved in increases in the serum levels of various enzymes and components in rats with WIRS. Rats were exposed to WIRS for 6 h after oral administration of vitamin E (VE) (50 or 250 mg/kg). Rats with WIRS had increased serum alanine aminotransferase, aspartate aminotranseferase, lactate dehydrogenase, creatine kinase, urea nitrogen, creatinine, glucose, corticosterone, adrenocorticotropic hormone and lipid peroxide (LPO) levels, increased kidney and heart VE levels, decreased skeletal muscle VE level, and increased LPO levels in all tissues studied. Pre-administered VE (50 or 250 mg/kg) attenuated the increased serum alanine aminotransferase, aspartate aminotranseferase, lactate dehydrogenase, creatine kinase, urea nitrogen, creatinine, and LPO levels, the decreased skeletal muscle VE level, and the increased LPO levels in all tissues studied more effectively at its higher dose than at its lower dose. However, either dose of the pre-administered VE did not affect the increased serum glucose, corticosterone, and adrenocorticotropic hormone levels. These results suggest that oxidative stress is involved in increases in the serum levels of various enzymes and components in rats with WIRS.