Predictor of buckwheat allergy in children based on challenge test results: a retrospective observational study in Japan.

Summary: Background. Buckwheat (BW) is a major food allergen and one of the leading causes of food-induced anaphylaxis in Japan. The standard method of diagnosing food allergy is the oral food challenge (OFC). The BW-specific IgE (BW-sIgE) value is used to assess BW allergy but its utility is limited. Aim. The aim of the present study was to identify factors with predictive value for the diagnosis of BW allergy using the OFC. Methods. We evaluated 37 patients who were classified into the positive or negative group according to their OFC results. Results. Ten patients (27.0%) showed objective or persistent, moderate, subjective symptoms during the OFC. The positive group had a significantly higher BW-sIgE/total IgE ratio than the negative group (p less than 0.001), but the total IgE (p = 0.139) and BW-sIgE (p = 0.130) did not differ significantly. Receiver operator characteristic (ROC) analysis showed that the BW-sIgE/total IgE ratio had a larger area under the curve (AUC, 0.885) than BW-sIgE (AUC, 0.667). The statistically optimal cut-off was 0.0058 for the BW-sIgE/total IgE ratio, which corresponded to a clinical sensitivity and specificity of 90.0% and 81.5%, respectively. Conclusions. BW-sIgE/total IgE ratio may be more useful predictor of BW OFC results than BWs-IgE.

Effects of Low-Dose Dairy Protein Plus Micronutrient Supplementation during Resistance Exercise on Muscle Mass and Physical Performance in Older Adults: A Randomized, Controlled Trial.

OBJECTIVES: To investigate whether supplementation with low-dose dairy protein plus micronutrients augments the effects of resistance exercise (RE) on muscle mass and physical performance compared with RE alone among older adults. DESIGN: Randomized controlled trial. SETTING: Tokyo, Japan. PARTICIPANTS: Eighty-two community-dwelling older adults (mean age, 73.5 years) were randomly allocated to an RE plus dairy protein and micronutrient supplementation group or an RE only group (n = 41 each). INTERVENTION: The RE plus supplementation group participants ingested supplements with dairy protein (10.5 g/day) and micronutrients (8.0 mg zinc, 12 µg vitamin B12, 200 µg folic acid, 200 IU vitamin D, and others/day). Both groups performed the same twice-weekly RE program for 12 weeks. MEASUREMENTS: Whole-body, appendicular, and leg lean soft-tissue mass (WBLM, ALM, and LLM, respectively) with dual-energy X-ray absorptiometry, physical performance, biochemical characteristics, nutritional intake, and physical activity were measured before and after the intervention. Data were analyzed by using linear mixed-effects models. RESULTS: The groups exhibited similar significant improvements in maximum gait speed, Timed Up-and-Go, and 5-repetition and 30-s chair stand tests. As compared with RE only, RE plus supplementation significantly increased WBLM (0.63 kg, 95% confidence interval [CI]: 0.31-0.95), ALM (0.37 kg, 95% CI: 0.16-0.58), LLM (0.27 kg, 95% CI: 0.10-0.46), and serum concentrations of 25-hydroxyvitamin D (4.7 ng/mL, 95% CI: 1.6-7.9), vitamin B12 (72.4 pg/mL, 95% CI: 12.9-131.9), and folic acid (12.9 ng/mL, 95% CI: 10.3-15.5) (all P < 0.05 for group-by-time interactions). Changes over time in physical activity and nutritional intake excluding the supplemented nutrients were similar between groups. CONCLUSION: Low-dose dairy protein plus micronutrient supplementation during RE significantly increased muscle mass in older adults but did not further improve physical performance.

Reduced hyperalgesia induced by nerve injury, but not by inflammation in mice lacking protein kinase C gamma isoform.

Protein kinase C is one of protein kinases which might be involved in the nerve injury- or inflammation-induced hyperalgesia. The present study was designed to investigate the hyperalgesia with thermal paw-withdrawal test induced by sciatic nerve ligation or by intraplantar injection of a complete Freund's adjuvant solution in protein kinase C gamma knockout and its wild-type mice. Either sciatic nerve ligation or intraplantar injection of a complete Freund's adjuvant caused a marked decrease of the paw-withdrawal latency only on the ipsilateral, but not on the contralateral side of the paw in wild-type mice. This ipsilateral hyperalgesia induced by sciatic nerve ligation was significantly attenuated in protein kinase C gamma knockout mice. On the other hand, the ipsilateral hyperalgesia induced by complete Freund's adjuvant remained about the same in protein kinase C gamma knockout mice as in wild-type mice. The results indicate that protein kinase C gamma is involved in the development of the thermal hyperalgesia induced by nerve ligation, but not by complete Freund's adjuvant-induced inflammation.

Changes in Ca2+-dependent protein kinase C isoforms induced by chronic ethanol treatment in mice.

Protein kinase C (PKC) has been shown to regulate ethanol sensitivity. The goal of the present study was to ascertain whether chronic in vivo ethanol treatment could affect PKC isoforms in the mouse brain. We measured the protein level of membrane-bound PKC isoforms following chronic ethanol treatment using Western blotting. The protein level of membrane-bound PKCalpha and PKCgamma isoforms, which are defined as Ca2+-dependent PKC isoforms (cPKC), in the limbic forebrain during chronic ethanol treatment was significantly increased, whereas the levels of both were significantly decreased in the frontal cortex. By contrast, there was no change in PKCepsilon, a Ca2+-independent PKC isoform, in both areas. These findings suggest that the change in membrane-bound cPKC in the limbic forebrain and frontal cortex may play substantial roles for the development of ethanol dependence.

Calcium supplement increase on the second day of sequential two day leukapheresis.

Peripheral blood progenitor cells are collected effectively by leukapheresis of a large volume of peripheral blood. However, protection must be taken for patients or donors from hypocalcemia due to continuous infusion of citric acid. We found a tendency for hypocalcemic symptoms in patients or donors to occur more often on the second day than the first day of the sequential 2 days of leukapheresis. The doses of calcium gluconate supplement and the acid citrate dextrose-A solution administration significantly increased on the second day compared to that of the first day. The blood levels of c-terminal parathormone (PTH), phosphorus, and alkaline phosphatase did not show remarkably abnormal change. However, urine calcium excretion just after leukapheresis was higher than in the period before or after leukapheresis compared to the phosphorus or creatinine excretion. These findings indicate that the cause of a higher tendency to hypocalcemic symptoms on the second day of the sequential 2 days of leukapheresis is due to the higher metabolism of calcium being excreted in the urine during leukapheresis.

Involvement of spinal protein kinase C in thermal hyperalgesia evoked by partial sciatic nerve ligation, but not by inflammation in the mouse.

Activation of several protein kinases contributes to the development of hyperalgesia evoked by injuries. The present study was designed to investigate the role of protein kinase C in the spinal cord in thermal hyperalgesia evoked by sciatic nerve ligation or by intraplantar injection of complete Freund's adjuvant. The paw withdrawal latency on the ipsilateral side, but not on the contralateral side, was markedly decreased after sciatic nerve ligation. Intraplantar injection of complete Freund's adjuvant also caused markedly decreases of the paw withdrawal latency. Intrathecal pretreatment with protein kinase C inhibitor calphostin C (100 and 250 ng) attenuated the decrease of the paw withdrawal latency evoked by sciatic nerve ligation. In contrast, the decrease of the paw withdrawal latency evoked by inflammation was only slightly attenuated by intrathecal pretreatment with calphostin C. The results indicate that protein kinase C in the spinal cord is involved in the development of the thermal hyperalgesia evoked by nerve ligation and is much less involved in the thermal hyperalgesia by complete Freund's adjuvant's-induced inflammation.

[Clinical evaluation of kampo medication, mainly with wen-pi-tang, on the progression of chronic renal failure].

Previous studies have shown that Kampo (traditional Chinese) prescriptions, mainly Wen-Pi-Tang (Onpi-to, [symbol see: text]), have a useful effect in patients with chronic renal failure (CRF). We aimed to examine the long-term effect of Kampo prescriptions on serum creatinine (Cr) among patients with CRF. Patients with serum Cr levels of 2 mg/dl more were enrolled if they had at least 4 recordings of serum Cr in the previous 6 months or more, and were followed-up until the start of dialysis. Eight patients aged 24-59 years with serum Cr 4.5 mg/dl were enrolled in the study for 40 to 402 weeks (mean; 228.1 +/- 118.8 weeks). The cause of CRF was chronic glomerulonephritis in 7 patients and systemic lupus erythematosus in 1 patient. The end points of the study were the slope of the reciprocal of the serum Cr concentration plot against time using Mitch's method, and the predicted period of pre-dialysis. The predicted pre-dialysis period was defined as an increase in serum Cr by 10 mg/dl. As a result, the individual slopes were improved in 6 of 8 cases, in particular, in 4 of 5 Wen-Pi Tang-treated cases. The average slope was improved significantly (p < 0.01) in Wen-Pi-Tang-treated cases, although it showed only a tendency to improve in all 8 cases. The predicted pre-dialysis period was prolonged from 79.2 +/- 74.8 weeks to 389.5 +/- 355.4 weeks and 55.6 +/- 37.0 weeks to 262.4 +/- 145.8 weeks in all 8 cases and Wen-Pi-Tang-treated cases, respectively. The observed pre-dialysis period was 228.1 +/- 118.8 weeks, which showed that Kampo prescriptions prolonged the predicted period for 186 additional weeks. In conclusion, this study demonstrated that the Kampo prescriptions, consisting mainly of Wen-Pi-Tang, retarded the progression of CRF.

Overproduction of antiplatelet antibody against glycoprotein IIb after splenectomy in a patient with Evans syndrome resulting in acquired thrombasthenia.

We treated a 33-year-old female with Evans syndrome. She received high dose gamma globulin, prednisolone, and azathioprine, and her platelet count transiently increased. After splenectomy, the platelet count markedly increased. However, the bleeding tendency worsened and the bleeding time was prolonged. A platelet defect, characteristic of thrombasthenia, was found. Antigen-captured ELISA and Western blotting revealed that the patient's serum had an IgG autoantibody against platelet membrane glycoprotein IIb and the patient's plasma inhibited normal platelet aggregation. These findings suggest that overproduction of the antiplatelet antibody is triggered by platelet recovery due to splenectomy and affects platelet function resulting in acquired thrombasthenia.

Blockade of late-phase airway responses and airway hyperresponsiveness in allergic sheep with a small-molecule peptide inhibitor of VLA-4.

The leukocyte integrin very late antigen-4 (VLA-4) (alpha 4 beta 1, CD49d/CD29) is an adhesion receptor predominantly expressed on lymphocytes, monocytes, and eosinophils, but not on neutrophils. Recent studies with monoclonal antibodies against VLA-4 suggest that antigen-induced late responses and airway hyperresponsiveness (AHR) may depend on the recruitment and/or activation of VLA-4-expressing leukocytes. To further test this hypothesis, we administered by aerosol either a potent small-molecule inhibitor of VLA-4, which prevents VLA-4-mediated binding to fibronectin (CS-1 ligand mimic), or an inactive control (30 mg twice daily for 3 d, and on the fourth day 0.5 h before and 4 h after antigen challenge) to six sheep with airway hypersensitivity to Ascaris suum antigen. Treatment with the small-molecule VLA-4 inhibitor resulted in a significant decrease in the early antigen-induced bronchial response (40%, p < 0.05), and almost complete blockade of the late-phase airway response (88%, p < 0.05). Moreover, at 24 h after antigen challenge, AHR to inhaled carbachol was not observed when the animals were dosed with the small-molecule VLA-4 inhibitor. In accord with protection against the functional abnormalities associated with antigen challenge, analysis of biopsy specimens taken 24 h after challenge indicated that the total numbers of VLA-4-positive cells (lymphocytes, eosinophils, and metachromatic-staining cells) in the group treated with the VLA-4 inhibitor did not increase, whereas these cells increased in the control group. The active agent, but not the inactive control, significantly blocked macrophage adherence to fibronectin (FN), indicating that the CS-1 ligand interfered with VLA-4-mediated adhesion in sheep cells. These results support our previous findings with a monoclonal antibody to VLA-4, and demonstrate that a small-molecule VLA-4 inhibitor, when given by aerosol, has a protective effect against antigen-induced late responses and AHR in allergic sheep.

Inhibition of UDP-glucuronosyltransferase by aglycons of natural glucuronides in kampo medicines using SN-38 as a substrate.

7-Ethyl-10-[4-(piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11), a potent anticancer agent for lung and gynecological cancers, is metabolized in vivo to the active compound, 7-ethyl-10-hydroxycamptothecin (SN-38), which is subsequently conjugated to SN-38-glucuronide by UDP-glucuronosyltransferase (UDP-GT). Three purified aglycons of natural glucuronides, baicalein, luteolin and glycyrrhetic acid, inhibited UDP-GT activity towards SN-38 as a substrate. The inhibitory potencies of these aglycons toward UDP-GT were similar to that of 1-naphthol. Based on these results, together with our previous finding that the corresponding glucuronides used in the present study strongly inhibited beta-glucuronidase in gut flora, we propose that materials in Kampo (Japanese herbal) medicines containing these aglycons of natural glucuronides could be used in vivo to decrease the enterohepatic circulation of SN-38 and other drugs.

Desensitization of capsaicin-sensitive sensory neurons in rat stomachs on chronic treatment with sodium taurocholate.

We examined the effects of chronic treatment with 10 mM sodium taurocholate (TC) on gastric functions, capsaicin-sensitive afferent neurons and the gastric mucosa in male rats. Stomachs were mounted in Lucite chambers, and then the transmucosal potential difference (PD), luminal pH and gastric mucosal blood flow (GMBF) in response to TC or capsaicin was determined. In normal animals, 10 mM TC caused a reduction in PD, and increases in luminal pH and GMBF. Capsaicin (1 mg/ml) produced an apparent increase in GMBF without any change in PD or luminal pH. After 4- or 12-week treatment with TC, the basal PD was significantly reduced, and the luminal pH tended to increase. The increase in GMBF in response to TC or capsaicin was profoundly suppressed in TC-pretreated animals. The calcitonin gene-related peptide release in response to capsaicin was significantly reduced after 4 weeks treatment with TC. There were no microscopical changes in the oxyntic mucosa until 4 weeks after TC treatment except for exfoliation of surface cells. However, an increase in inflammatory cell infiltration was observed 12 weeks later. We conclude that chronic treatment with TC causes desensitization of capsaicin-sensitive afferent neurons and reduces GMBF, which may result in the production of gastritis.

[Quantitative analysis of 123I-metaiodobenzylguanidine myocardial imaging: assessment of its usefulness in patients with congestive heart failure].

To investigate the usefulness of the quantitative analysis of 123I-metaiodobenzylguanidine (123I-MIBG) myocardial uptake, we studied 9 normal subjects and 18 patients with congestive heart failure (CHF). Rest myocardial imaging with 123I-MIBG was performed at 20 minutes and 3 hours (delayed image) after 123I-MIBG injection. Rest 201Tl imaging was obtained at 20 minutes after 201Tl injection. In addition to ordinary tomograms, a planar anterior image and a whole body image were supplemented in each imaging. In patients with CHF fractional shortening (%FS) was calculated from echocardiography and left ventricular ejection fraction was obtained from cardiac blood pool imaging with 99mTc at rest. We calculated H/M (heart to mediastinum count ratio) from the anterior planar image and %Uptake (percentage of cardiac uptake of the isotope to total injected dose) from the whole body image. H/M of 123I-MIBG in delayed images separated patients with CHF from normal subjects (2.00 +/- 0.19 vs. 2.56 +/- 0.13, p < 0.01). H/M Ratio (H/M of 123I-MIBG divided by H/M of 201Tl) in delayed image could distinguish these two groups poorly (0.72 +/- 0.12 vs. 0.88 +/- 0.14, p < 0.05). On the other hand, %Uptake of 123I-MIBG was not different between two groups (3.49 +/- 0.60% in CHF, 3.54 +/- 0.34% in normal). But %Uptake of 201Tl was greater in CHF than in normal (5.96 +/- 1.09% vs. 4.70 +/- 0.30%, p < 0.05). When myocardial 123I-MIBG uptake was normalized by myocardial perfusion (%Uptake of 123I-MIBG divided by %Uptake of 201Tl, Uptake Ratio), Uptake Ratio in delayed image could distinguish theses two groups as same as H/M (0.60 +/- 0.05 in CHF, 0.75 +/- 0.05 in normal, p < 0.01). In patients with CHF, H/M of 123I-MIBG did not reflect LV function and serum norepinephrine (NE) level. But Uptake Ratio and H/M Ratio in delayed image correlated well with %FS (r = 0.88, r = 0.65), EF (r = 0.80, r = 0.68) and NE level (r = -0.77, r = -0.75). Although the calculation of Uptake Ratio is time consuming and expensive, it was assumed that Uptake Ratio is an useful index to quantitate myocardial 123I-MIBG uptake.

[Cutaneous or subcutaneous calcinosis observed in leprosy patients. 1. Clinical observations].

A roentgenographic examination was made for the limbs of leprosy patients with calcinosis in whom atrophic cutaneous sclerosis and subcutaneous induration or infiltration were observed. The observation results are summarized as follows. 1. Atrophic cutaneous sclerosis was one of a sequela in lepromatous lesion, especially in case of ENL, and it was observed to occur frequently at the extended sides of 1/3distal part from the forearm and the crus mainly. The atrophied cutaneous surface was tinged with lustrous red. It was able to observe calcium deposition directly just under the skin and/or in the shallow subcutaneous region from the roentgenogram of the site. The roentgenographic patterns were demonstrated as if many granules were scattered, and also the dendric and reticular platy-expansions were detected in some cases. The enucleated parts seemed to be similar to the cancellous bone. It might be said that dystrophic calcinosis cutis developed by inducing histological disorder is one of the origin of such a calcinosis, because the skin in these regions is deficient in the mobility and tends to provoke the circulatory disorder in case of chronic inflammation as discerned in lepromatous lesion. 2. An induration in subcutaneous tissue is lipid lump being as it was when chaulmoogra oil was injected and not undergo absorption of the oil. The lipid lumps enveloped in the tunic were observed in the site of lateral upperarm and the front of femur. They seemed to be remained almost all as it was. It was observed that the lipid lumps, as such, were adjacent to the outer layer of fascia, but not in the muscle. And there are some cases where the oil flowed from the injection site through the hypodermis and got the lipid lumps formed in the forearm and/or the crus. Roentgenogram of that showed the existence of calcinosis regardless of size which transmissivity of X-ray had an irregular pattern. The enucleated lipid lumps were easily cut to pieces by scalpel. 3. It may be said that the calcinosis observed in atrophic cutaneous sclerosis due to lepromatous lesion or lipid lump of unabsorbed chaulmoogra oil makes it necessary for its healing to be 10-20 years. 4. Roentgenogram at that time revealed no abnormality as to serum calcium, phosphorous and/or alkaline phosphatase values.

Inhibition of beta-glucuronidase by natural glucuronides of kampo medicines using glucuronide of SN-38 (7-ethyl-10-hydroxycamptothecin) as a substrate.

1. 7-Ethyl-10-[4-(piperidino)-1-piperidino] carbonyloxycamptothecin (CPT-11), a potent anticancer agent currently under development for clinical use, is metabolized in vivo to 7-ethyl-10-hydroxycamptothecin (SN-38), which is subsequently conjugated to 7-ethyl-10-hydroxycamptothecin glucuronide (SN-38-glucuronide). The SN-38-glucuronide was hydrolysed by beta-glucuronidase from E. coli to aglycones and glucuronic acid. 2. Four purified natural glucuronides including baicalin, wogonoside, luteolin-3'-glucuronide, and glycyrrhizin, inhibited beta-glucuronidase using SN-38-glucuronide as substrate. The inhibition potencies of these natural glucuronides toward beta-glucuronidase were similar to that of saccharic acid 1,4-lactone. 3. These results indicate that plant materials of Kampo (Japanese herbal) medicines containing these glucuronides could be used in vivo to decrease the enterohepatic circulation of SN-38 and possibly that of other drugs.

Parasympatholytic effects of vecuronium are mediated by nicotinic and muscarinic receptors in hearts of anesthetized dogs.

We investigated the blocking effects of vecuronium and pancuronium on the negative chronotropic and dromotropic responses to stimulation of the parasympathetic nerves in the anesthetized, open-chest dog. We stimulated the intracardiac parasympathetic nerves to the SA nodal region (SAP stimulation) or to the atrioventricular nodal region (AVP stimulation). SAP stimulation or AVP stimulation selectively decreased heart rate or increased atrioventricular conduction time, respectively. Vecuronium and pancuronium inhibited the chronotropic response to SAP stimulation and the dromotropic response to AVP stimulation in a dose-dependent manner. The ID50 of each drug for the dromotropic response was less than that for the chronotropic response. The blocking effect of vecuronium on the negative cardiac responses to parasympathetic stimulation was about 10-fold less potent than that of pancuronium. These results suggest that the blocking effects of vecuronium and pancuronium on the negative chronotropic and dromotropic responses to parasympathetic stimulation differ from those of atropine in the heart. In the isolated right atrium perfused with blood from the support dog, vecuronium, injected into the external jugular vein of the support dog, dose-dependently inhibited the negative chronotropic and inotropic responses to carbachol or SAP stimulation and the negative followed by positive chronotropic and inotropic responses to nicotine. The ID50 values for carbachol, nicotine and SAP stimulation were not significantly different. These results suggest that parasympatholytic effects of vecuronium are mediated by not only muscarinic receptors but also neuronal nicotinic receptors in hearts of anesthetized dogs.

[Urinary excretion rate of methylguanidine as a new maker of active oxygen in vivo: demonstration in hyperbaric oxygen therapy].

Methylguanidine (MG) which is known as a uremic toxin, is synthesized from creatinine (Cre). We have clarified that active oxygen plays an important role on MG synthesis in vitro and in rat hepatocytes. On the other hand, hyperoxia is very injurious in various tissues, and it has been reported that active oxygen produced in hyperoxia plays an important role on the tissue injury. This study was performed to investigate the effect of hyperoxia on MG synthesis in vivo. The subjects in this study were patients who were treated by hyperbaric oxygen therapy (HBO). Serum Cre, MG, and urinary Cre, MG before and after HBO were measured in these subjects. The subjects were classified into four groups. Group I-III were undergone HBO with condition of 100% O2, 2 atmosphere absolute (ATA), 1 hour, (I: Ccr less than 10 ml/min, II: 10 less than or equal to Ccr less than 50 ml/min, III: Ccr greater than or equal to 50 ml/min) and group IV (Ccr greater than or equal to 50 ml/min) with 100%O2, 3ATA, 1 hour. Urinary excretion rate of MG (urine MG/urine Cre) significantly increased after HBO therapy in every group. Urine MG/urine Cre/serum Cre ratio which was used as a index of MG synthesis rate also increased. In this study, it is clarified that MG excretion rate increases in hyperoxic condition. These results suggest that active oxygen plays an important role on MG synthesis in vivo, and that the urine MG/urine Cre/serum Cre ratio can be a useful maker of the active oxygen products in vivo.

Comparative pathology of HPCD pigs infected with wild-type and ara-T-resistant strains of Aujeszky's disease virus.

Fourteen 1- to 4-week-old hysterectomy-produced and colostrum-deprived (HPCD) pigs were inoculated intranasally with wild-type and ara-T-resistant strains of Aujeszky's disease virus (ADV), and the pathological lesion induced by the two strains was compared. The wild-type strain (YS-81) led to high mortality, and the pigs developed multifocal necrosis throughout the body and encephalitis. In comparison, the ara-T-resistant strain (YS-81TR) of the virus killed only 1-week-old HPCD pigs inoculated with 10(6.0) PFU per ml of the virus and did not kill pigs more than 2-weeks of age. The latter revealed consistently severe pneumonitis on post-inoculation day (PID) 14. Results of the present study indicated that the ara-T-resistant strain of ADV was less virulent for HPCD pigs than the parental wild-type strain of ADV and that it was able to grow better in the lung than in any other tissue.

Protective effects of superoxide dismutase on acute reperfusion injury of gerbil brain.

It has been postulated that oxygen-derived free radicals are produced in significant quantities upon reperfusion of ischemic brain and could cause brain edema and cell death. This study was undertaken in an attempt to examine the effect of recombinant human superoxide dismutase, a scavenger of superoxide radicals, on survival outcome and brain edema in gerbils undergoing 1-hour bilateral carotid occlusion and reperfusion. Superoxide dismutase was continuously infused over either 1 or 3 h of reperfusion. Neither low dose (100,000 U/kg bolus followed by 100,000 U/kg/h continuous infusion) nor high dose (100,000 U/kg bolus followed by 800,000 U/kg/h) recombinant human superoxide dismutase had an effect upon water and sodium content of whole brain at 1 h of reperfusion following 1 h of ischemia, but high-dose treatment effectively reduced brain water content at 3 h of reperfusion. All gerbils receiving high-dose treatment survived the 3 h of reperfusion, while 4 of the 7 gerbils in the control group died between 2 and 3 h of reperfusion (p less than 0.05). From this study, we conclude that prophylactic administration of superoxide dismutase can reduce the delayed vasogenic edema developing at 3 h of reperfusion and afford significant cerebroprotection in these models of transient global ischemia.

Pathological changes in HPCD pigs with prednisolone induced recrudescence of pseudorabies virus.

In HPCD pigs inoculated with PRV, latent PRV could be reactivated in-vivo by the administration of large doses of prednisolone 3 months after the primary infection. In two pigs, virus shedding was without clinical signs of disease, whereas depression of circulating lymphocytes was prominent. Reactivation of PRV was also demonstrated by cultivation of the brain cortex on the 7th day and the mandibular lymph node on the 9th day after the prednisolone began treatment. Coincident with the virus isolation, characteristic lesions were observed in 2 pigs in the central nervous tissues and mandibular lymph nodes and these were composed of cell necrosis and eosinophilic intranuclear inclusion bodies. Cells containing the intranuclear inclusion bodies had immature and mature PRV particles. Results of the present study with HPCD pigs indicated that the lesions in the brain and lymph node accompanied by eosinophilic intranuclear inclusion bodies were pathogonomonic lesions induced by reactivation of PRV.