Biomedical subjects

H Wada

Publications and source records attributed to H Wada.

At least 181 records · Page 10Linked to original sources

PubMed2000

Suppression of neurocognitive damage in LP-BM5-infected mice with a targeted deletion of the TNF-alpha gene.

Brain levels of TNF-alpha increase in many inflammatory conditions, including HIV-1 infection, and may contribute to neurodegenerative processes. The paucity of agents that can selectively and potently block TNF-alpha processing or its receptors has led us to investigate the role of TNF-alpha in chronic neurodegeneration associated with retroviral infection using mice with targeted deletions of the TNF-alpha gene. Infection of wild-type C57BL/6 mice with the LP-BM5 murine leukemia retrovirus mixture leads to the development of a severe immunodeficiency as well as cognitive deficits and neuronal damage. TNF-alpha-(-/-) mice infected with LP-BM5 developed a systemic immunopathology indistinguishable in severity from that observed in contemporaneously infected wild-type mice. In contrast, the performance of infected TNF-alpha-(-/-) mice in the Y-maze and Morris water maze was not different from that of uninfected TNF-alpha-(-/-) mice. The extent of glial activation in the striatum, as indicated by the increase in density of peripheral benzodiazepine receptors, was equivalent in both groups of LP-BM5-infected mice. However, the decrease in striatal MAP-2 expression, a marker of neurodegeneration observed in infected wild-type mice, was not found in infected TNF-alpha-(-/-) mice. While the loss of TNF-alpha appeared to have no effect on the course or severity of the central or peripheral immunopathology resulting from LP-BM5 infection, the behavioral and biochemical manifestations were substantially curtailed in the TNF-alpha-(-/-) mice. These findings directly support a role for TNF-alpha in the neurodegenerative processes associated with viral infections such as HIV-1.

Animals↗

PubMed2000

Prognostic significance of proliferative activity in pN2 non-small-cell lung carcinomas and their mediastinal lymph node metastases.

OBJECTIVE: To investigate the expression of proliferating cell nuclear antigen (PCNA) in both primary tumor and lymph node metastases of pathologic stage IIIA N2 non-small-cell lung carcinoma (NSCLC) and the relation to prognosis. SUMMARY BACKGROUND DATA: Although the prognosis of pN2 NSCLC is poor in general, long-term survivors have been reported among patients with completely resected or clinical N0 disease and those with skip metastasis. However, few reports are available on preoperative prognostic predictors. Expression of PCNA is known to be associated with tumor proliferation and is correlated with the prognosis of several carcinomas. METHODS: Clinicopathologic factors were investigated in relation to prognosis in 76 patients with pathologic stage IIIA pN2 NSCLC from whom resected surgical specimens were available from both the primary tumor and lymph node metastases for evaluation of PCNA expression. RESULTS: A significant correlation was observed between PCNA labeling index in the primary tumor and that in lymph node metastases. The prognosis in patients with PCNA-negative primary tumor (5-year survival rate, 66.0%) was significantly more favorable than that of patients with PCNA-positive primary tumor (5-year survival rate, 21.5%). The prognosis in patients with PCNA-negative metastases was significantly more favorable than that of patients with PCNA-positive metastases. For clinical N2 disease also, the prognosis of patients with PCNA-negative primary tumor was favorable (5-year survival rate, 66.1%). Multivariate analyses showed that PCNA expression and complete resection were significant prognostic factors. CONCLUSIONS: Preoperatively diagnosed N2 NSCLC exhibiting negative PCNA expression in primary tumor or lymph node metastases is expected to result in a favorable postoperative prognosis and may be an indication for primary resection.

Aged↗

PubMed2000

Description of compensated and uncompensated disseminated intravascular coagulation (DIC) responses (non-overt and overt DIC) in baboon models of intravenous and intraperitoneal Escherichia coli sepsis and in the human model of endotoxemia: toward a better definition of DIC.

OBJECTIVE: Work toward a better definition of disseminated intravascular coagulation (DIC) by characterizing the difference between compensated and uncompensated responses of the hemostatic system to inflammatory stress in baboons and human subjects using global coagulation and molecular marker assays of hemostatic, inflammatory, and endothelial perturbation. DESIGN: We conducted prospective evaluation of the response of baboons to increasing concentrations of intravenous Escherichia coli, human subjects to intravenous endotoxin, and baboons to intraperitoneal E. coli. SETTING: Animal laboratory and medical intensive care facilities, University of Oklahoma Medical School laboratories. SUBJECTS: Cynocephalus baboons; normal healthy male human subjects (age, 24-37 yrs). MEASUREMENTS AND MAIN RESULTS: Global coagulation assays, white blood cell counts, and molecular marker assays (ELISA) of components of the inflammatory and hemostatic systems, neutrophil release products, and endothelial injury. A fall in both fibrinogen concentration and platelet counts indicated a decompensated hemostatic response to inflammatory stress (ie, overt DIC). These responses were observed 2-6 hrs after intravenous infusion of 10(9) and 10(10) colony-forming units (CFU)/g of E. coli and after implantation of 10(11) CFU/g of E. coli into the peritoneal cavity. However, 6 hrs after E. coli challenge, these tests were much less reliable as markers of overt DIC because the fibrinogen underwent an acute phase response and the platelet count fell and remained depressed for 48 hrs in the face of a coagulopathic response that was already beginning to resolve, as reflected by a rising fibrinogen concentration. This lack of reliability was particularly evident in the E. coli peritonitis studies, in which one third of the animals recovered, one third remained sick for up to 14 days, and one third died. In contrast, fibrin degradation products and the molecular markers thrombin/antithrombin, soluble fibrin monomer, protein C, and activated protein C/inhibitor complexes responded consistently in a dose-dependent manner regardless of the length of time after challenge. These variables exhibited this dose response to 106 and 108 CFU/g of E. coli in absence of a fall in fibrinogen concentration. This was defined as a compensated hemostatic response to inflammatory stress (ie, non-overt DIC). The values of these variables correlated closely with rising concentrations of markers of neutrophil activation (elastase/alpha 1 antitrypsin) and endothelial injury (soluble thrombomodulin). This was particularly evident in the human response to endotoxin, in which there was abundant evidence of hemostatic marker response in absence of a fall in platelet or fibrinogen concentration, both immediately after endotoxin infusion (first stage, 0-8 hrs after endotoxin) and later (second stage, 12-48 hrs after endotoxin). CONCLUSION: Global coagulation tests are most useful in detecting overt consumptive coagulopathy (overt DIC) near the time of challenge or injury (1 to 6 hrs). Molecular markers can detect and grade the degree of hemostatic stress of a non-overt consumptive coagulopathy (nonovert DIC). These markers correlate with degree of endothelial cell injury and reveal a reperfusion injury stage (second stage) in the human endotoxin model of compensated hemostatic stress after all clinical symptoms have subsided and the subjects have returned to work.

Animals↗

PubMed2000

Direct evidence for requirement of phosphatidylglycerol in photosystem II of photosynthesis.

Phosphatidylglycerol (PG) is considered to play an important role in the ordered assembly and structural maintenance of the photosynthetic apparatus in thylakoid membranes. However, its function in photosynthesis remains poorly understood. In this study we have identified a pgsA gene of Synechocystis sp. PCC6803 that encodes a PG phosphate synthase involved in the biosynthesis of PG. A disruption of the pgsA gene allowed us to manipulate the content of PG in thylakoid membranes and to investigate the function of PG in photosynthesis. The obtained pgsA mutant could grow only in the medium containing PG, and the photosynthetic activity of the pgsA mutant dramatically decreased with a concomitant decrease of PG content in thylakoid membranes when the cells grown in the presence of PG were transferred to the medium without PG. This decrease of photosynthetic activity was attributed to the decrease of photosystem (PS)II activity, but not to the decrease in PSI activity. These findings demonstrate that PG is essential for growth of Synechocystis sp. PCC6803 and provide the first direct evidence that PG plays an important role in PSII.

Amino Acid Sequence↗

PubMed2000

Molecular and biological analysis of carcinoma of the small intestine: beta-catenin gene mutation by interstitial deletion involving exon 3 and replication error phenotype.

The genetic mechanisms of carcinomas of the small intestine are not well understood. We report the results of analysis of genetic alterations in a case of small intestinal carcinoma. A tumor in the terminal ileum was resected in a 59-yr-old woman. Histologically, the tumor was classified as well-differentiated adenocarcinoma. We screened for genetic alterations in adenomatous polyposis coli (APC), beta-catenin, K-ras, and p53 genes, as well as microsatellite instability, which are known to be involved in colorectal tumorigenesis. The tumor exhibited somatic interstitial deletion of 425-bp, which included the entire exon 3 in beta-catenin gene. Immunohistochemical staining confirmed accumulation of aberrant beta-catenin protein in the cytoplasm and nuclei of the malignant tissue. Furthermore, a frameshift mutation in the transforming growth factor beta receptor type II gene with replication error phenotype was detected in the tumor DNA. In contrast, no genetic alterations were found in the APC, K-ras, and p53 genes. Our results suggested that both beta-catenin gene mutation and replication error phenotype might contribute to carcinogenesis of the small intestinal tumor in our case. This is the first report that activation of beta-catenin gene by somatic gene mutation is involved in the development of carcinoma of the small intestine.

Amino Acid Sequence↗

PubMed2000

Mechanism of increases in L-kynurenine and quinolinic acid in renal insufficiency.

Marked increases in metabolites of the L-tryptophan-kynurenine pathway, L-kynurenine and quinolinic acid (Quin), were observed in serum and cerebrospinal fluid (CSF) of both the rat and human with renal insufficiency. The mechanisms responsible for their accumulation after renal insufficiency were investigated. In patients with chronic renal insufficiency, elevated levels of serum L-kynurenine and Quin were reduced by hemodialysis. In renal-insufficient rats, Quin and L-kynurenine levels in serum, brain, and CSF were also increased parallel to the severity of renal insufficiency. Urinary excretion of Quin (3.5-fold) and L-kynurenine (2.8-fold) was also increased. Liver L-tryptophan 2,3-dioxygenase activity (TDO), a rate-limiting enzyme of the kynurenine pathway, was increased in proportion to blood urea nitrogen and creatinine levels. Kynurenine 3-hydroxylase and quinolinic acid phosphoribosyltransferase were unchanged, but the activities of kynureninase, 3-hydroxyanthranilate dioxygenase, and aminocarboxymuconate-semialdehyde decarboxylase (ACMSDase) were significantly decreased. Systemic administrations of pyrazinamide (ACMSDase inhibitor) increased serum Quin concentrations in control rats, demonstrating that changes in body ACMSDase activities in response to renal insufficiency are important factors for the determination of serum Quin concentrations. We hypothesize the following ideas: that increased serum L-kynurenine concentrations are mainly due to the increased TDO and decreased kynureninase activities in the liver and increased serum Quin concentrations are due to the decreased ACMSDase activities in the body after renal insufficiency. The accumulation of CSF L-kynurenine is caused by the entry of increased serum L-kynurenine, and the accumulation of CSF Quin is secondary to Quin from plasma and/or Quin precursor into the brain.

Adult↗

PubMed2000

Effects of dibutyryl cyclic adenosine monophosphate on the ultrastructure of endothelial cells in rat lungs cold preserved for 15 hours.

BACKGROUND: Dibutyryl cyclic adenosine monophosphate (db-cAMP) has been shown to protect vascular endothelial cells by increasing the level of intracellular cAMP, and we have previously reported its effectiveness in lung preservation. Here, the effects of db-cAMP in lung preservation were ultrastructurally investigated, and the ultrastructural changes before reperfusion were correlated with pulmonary function after reperfusion. METHODS: The lungs of 17 Lewis rats were flushed with perfusate and prostaglandin E(1), and were then divided into three groups. In the fresh group (n = 6), the lungs were flushed with extracellular-type trehalose-containing (ET-K) solution and were reperfused immediately. In the control group (n = 6) and db-cAMP group (n = 5), the lungs were flushed with ET-K solution and ET-K solution plus db-cAMP (2 mM), respectively, and were reperfused after cold preservation at 4 degrees C for 15 h. Before reperfusion, tissue was sampled and ultrastructurally analyzed by transmission electron microscopy. RESULTS: In the endothelial cells of pulmonary arterioles, the incidence of protrusion was significantly lower in the fresh and db-cAMP groups than in the control group (p < 0.05). The incidence of detachment and microvillus formation were significantly lower in the fresh and db-cAMP groups than in the control group (p < 0.01). The ultrastructure of the alveoli did not allow separation of the control and db-cAMP groups. The shunt fraction and wet to dry weight ratio of the lung tissue after reperfusion were significantly lower in the fresh and db-cAMP groups than in the control group (p < 0.01). Positive correlations were found between the incidence of these ultrastructural changes in the endothelial cells of the pulmonary arterioles and pulmonary function after reperfusion. CONCLUSION: These findings suggest that db-cAMP might attenuate the lung injury caused by cold preservation and ischemia-reperfusion, partly by suppressing the acceleration of the structural changes in the endothelial cells in the pulmonary arterioles.

Animals↗

PubMed2000

Long-term administration of oral low-dose topoisomerase II inhibitors, MST-16 and VP-16, for refractory or relapsed non-Hodgkin's lymphoma.

It is known that the topoisomerase II inhibitors, MST-16 (sobuzoxane) and VP-16 (etoposide), are effective for the treatment of lymphoma. Five patients with refractory or relapsed non-Hodgkin's lymphoma (NHL) were treated with a combination of oral MST-16 and VP-16 over a long period. Two patients had severely refractory NHL. The remaining 3 patients could not be treated with intensive chemotherapy because of severe organ dysfunction or a poor hematopoietic reserve. All 5 are alive and well after MST-16 and VP-16 treatment. MST-16 and VP-16 are effective for NHL when intensive chemotherapy is ineffective or contraindicated.

Administration, Oral↗

PubMed2000

New imaging findings in a patient with central nervous system dysfunction after bone marrow transplantation.

Central nervous system disorders are an important complication of bone marrow transplantation (BMT). We have recently performed cerebral angiography to examine central nervous system dysfunction in a 22-year-old woman with acute lymphoblastic leukaemia who had undergone BMT. Angiography demonstrated multiple stenoses and occlusions in the peripheral branches of the anterior and middle cerebral arteries, a pattern similar to that seen in vasculitis. She was thought to most likely have cytomegalovirus (CMV) vasculitis, but other forms of vasculitis, such as angiitis-like-syndrome-associated graft-versus-host disease could not be excluded. This case suggests that CMV vasculitis may cause central nervous system dysfunction after BMT and that imaging studies may provide useful information about central nervous system disorders in these patients.

Adult↗

PubMed2000

Acute promyelocytic leukemia with marrow fibrosis at initial presentation: possible involvement of transforming growth factor-beta(1).

Although the occurrence of marrow fibrosis in acute myeloid leukemia has been described, there have been no reports of acute promyelocytic leukemia (APL) associated with marrow fibrosis. Here we describe an APL patient with severe marrow fibrosis at initial presentation. He had the typical manifestations of APL, except for marrow fibrosis. Complete remission was achieved by treatment with all-trans retinoic acid plus chemotherapy, and his marrow fibrosis gradually improved concomitantly with the decrease in leukemic cells. To clarify the mechanism of marrow fibrosis in this patient, we investigated the expression of genes for several cytokines promoting fibrosis by the reverse transcriptase polymerase chain reaction methods. An overexpression of transforming growth factor-beta(1) was noted in his leukemic cells at initial presentation, whereas no increase in expression was observed at the time of relapse when he no longer had marrow fibrosis. These findings suggest that overexpression of transforming growth factor-beta(1) was involved in the development of marrow fibrosis in this APL patient.

Adult↗

PubMed2000

Cytoprotective effects of nitroglycerin in ischemia-reperfusion-induced lung injury.

Prevention of ischemia-reperfusion (IR) injury is crucial for successful lung transplantation. We investigated whether a nitric oxide donor, nitroglycerin (NTG), could suppress the oxidative stress of IR injury and improve pulmonary function after reperfusion in an ex vivo rat lung perfusion model. In Fresh group of animals, the lungs were flushed with perfusate, followed immediately by reperfusion, and no lung injury was observed. In NTG- and NTG+ groups of animals, the lungs were flushed with perfusate alone or perfusate containing NTG, respectively. Harvested lung and heart blocks from these latter two groups were immersed in the corresponding perfusate at 4 degrees C for 15 h, and were then reperfused for 60 min. Reperfusion induced pulmonary edema in the NTG- group, but not in the NTG+ group. Shunt fractions in NTG+ group were significantly lower than in the NTG- group throughout reperfusion. NTG had no effect on pulmonary arterial pressure or myeloperoxidase activity. In contrast, oxidative DNA damage assessed immunohistochemically with a monoclonal antibody against 8-hydroxy-2'-deoxyguanosine (8-OHdG) was significantly increased in the NTG- group, in the order alveolar epithelium > pulmonary endothelium > bronchial epithelium. NTG treatment significantly decreased staining with the anti-8-OHdG antibody in all three areas of tissue. Therefore, administration of NTG attenuates the oxidative stress of IR injury, and may improve pulmonary function after reperfusion.

Animals↗

PubMed2000

Elevated tissue factor levels in leukemic cell homogenate.

Tissue factor (TF) antigen and activity were measured in leukemic cell homogenates. In leukemic cell homogenate, especially that of acute promyelocytic leukemia (APL), both TF antigen and activity were significantly higher than these levels in the mononuclear cells obtained from healthy volunteers. Both TF antigen and activity were significantly higher in myelocytic leukemia than in lymphocytic leukemia cells. In leukemic cell homogenates, there was a close correlation between TF antigen and TF activity. The TF activity/TF antigen ratio was significantly higher in myelocytic leukemia than in lymphocytic leukemia cells. As the TF activity was not increased in lymphocytic leukemia cell homogenates to which were added phospholipids, the decrease in TF activity in lymphocytic leukemia might not be due to phospholipid in the leukemic cell membrane. Values for TF activity, TF antigen, and the TF activity/TF antigen ratio in leukemic cell homogenate from patients with disseminated intravascular coagulation (DIC) were significantly higher than those in patients without DIC. Therefore, the measurement of TF antigen and activity in leukemic cells could be useful for the prediction of DIC.

Antigens, Neoplasm↗

PubMed2000

Hemostatic abnormalities in patients with thrombotic complications on maintenance hemodialysis.

Before hemodialysis (HD), plasma levels of tissue factor (TF), free-TF pathway inhibitor (TFPI) and thrombomodulin (TM) were significantly higher in patients with HD than in healthy volunteers. Plasma levels of (T-F) TFPI and plasmin plasmin inhibitor complex (PPIC) were significantly higher in patients with HD than in healthy volunteers. During HD, plasma levels of TF and (T-F) TFPI were not significantly increased, but plasma levels of total TFPI and free TFPI at 1 hour after and at the end of HD were significantly increased, compared with levels before start of HD. Plasma level of PPIC 1 hour after start of HD was significantly higher than before start of HD, and plasma levels of thrombin antithrombin complex (TAT), PPIC, D-dimer, TM, and protein C (PC) at the end of HD were significantly higher than before start of HD. In patients with thrombosis complications, plasma TF levels were significantly higher than in patients without thrombotic complications during HD. Plasma levels of PC were significantly lower in patients with thrombotic complications than in patients without thrombotic complications. There was no significant difference between both groups during HD in hemostatic parameters, with the exception of TF and PC. Hemostatic abnormalities existed in patients with HD; especially, increased TF and decreased PC might cause thrombotic complications.

Antifibrinolytic Agents↗

PubMed2000

Coagulation tests and anti-phospholipid antibodies in patients positive for lupus anticoagulant.

We examined activated partial thromboplastin time, kaolin clotting time, mixing with normal plasma in kaolin clotting time, dilute Russell's viper venom time, dilute Russell's viper venom time at high lipid concentrations, anti-phospholipid antibodies, and anti-cardiolipin-beta2-glycoprotein I complex antibody in 135 patients with prolongation of activated partial thromboplastin time and diagnosed 86 patients positive for lupus anticoagulant. The sensitivity of activated partial thromboplastin time and dilute Russell's viper venom time/dilute Russell's viper venom time-high lipid concentrations ratio for lupus anticoagulant were markedly high, but the specificity of activated partial thromboplastin time for lupus anticoagulant was not markedly high. The specificity, but not the sensitivity, of kaolin clotting time-mixing with normal plasma in kaolin clotting time was markedly high. In summary, dilute Russell's viper venom time to dilute Russell's viper venom time-high lipid concentrations ratio gave high sensitivity as well as specificity, being the only assay to confirm this. Of the patients positive for lupus anticoagulant, 25% were positive for anti-phospholipid antibodies and 17% were positive for anti-cardiolipin-beta2-glycoprotein I complex antibody. Of the lupus anticoagulant-positive patients with thrombosis, 45% were positive for anti-phospholipid antibodies, 35% were positive for anti-cardiolipin-beta2-glycoprotein I complex antibody, 60% were positive for both anti-phospholipid antibodies and anti-cardiolipin-beta2-glycoprotein I complex antibody, and only 17% were negative for anti-phospholipid antibodies and anti-cardiolipin-beta2-glycoprotein I complex antibody. These findings suggest that lupus anticoagulant can be diagnosed by dilute Russell's viper venom time/dilute Russell's viper venom time-high lipid concentrations ratio, and that thrombosis in lupus anticoagulant-positive may be predictable from both anti-phospholipid antibodies and anti-cardiolipin-beta2-glycoprotein I complex antibody. Plasma tissue type plasminogen activator level in lupus anticoagulant patients was significantly increased, and plasma tissue type plasminogen activator and fibrin-D-dimer levels in lupus anticoagulant-positive patients with thrombosis were significantly higher than in those without thrombosis, suggesting that the diagnosis of thrombosis by hemostatic markers might be important in lupus anticoagulant.

Adult↗

PubMed2000

Changes of hemostatic molecular markers after gynecological surgery.

The authors evaluated the hemostatic abnormalities occurring in the postoperative period of eight patients with malignant tumors and compared them with those occurring in the postoperative period of eight patients with benign tumors. Two of the patients with malignant tumor presented pulmonary embolism after operation. Plasma fibrinogen and fibrin degradation product levels in patients with malignant tumors were already high before operation and further increased significantly after operation. The plasma levels of D-dimer, thrombin-antithrombin complex, and free-tissue factor pathway inhibitor were increased in both groups after operation, but they were higher in patients with malignant tumors than in patients with benign tumors. The plasma levels of protein C and antithrombin were significantly decreased in both groups after operation. but they were significantly lower in patients with malignant tumors than in those with benign tumors. The decreased activity of protein C or antithrombin may be not only a risk factor of thrombotic disease, such as pulmonary embolism, but also the cause of thrombosis. In patients with malignant tumors, the operation time was significantly longer than that in patients with benign tumors. This long operative period might cause vascular endothelial cell injury which is reflected by the plasma levels of free-tissue factor pathway inhibitor, antithrombin, and protein C.

Adult↗

PubMed2000

Decreased protein C activation is associated with abnormal collagen turnover in the intraalveolar space of patients with interstitial lung disease.

Activation of the coagulation system in the alveolar space plays an important role in the pathogenesis of interstitial lung disease (ILD) and pulmonary fibrosis. The protein C (PC) pathway is the main modulator of coagulation activation. This study evaluated whether dysfunction of the PC pathway is associated with increased collagen synthesis in the intraalveolar space of patients with ILD. This study comprised 22 patients with ILD; of these, five had idiopathic pulmonary fibrosis (IPF), nine had sarcoidosis-associated ILD, and eight had collagen vascular disease-associated ILD (CVD-ILD). Thrombin-antithrombin complex (TAT) was measured as a marker of coagulation activation. As markers of the PC pathway activity, the concentration of activated PC-PC inhibitor (APC-PCI) complex and the APC-PCI/PC ratio were measured and, as a marker of collagen synthesis, the concentration of aminoterminal propeptide of type III procollagen (PIIINP) was measured in bronchoalveolar lavage fluid (BALF) of ILD patients. TAT was significantly increased in BALF from ILD patients as compared to control subjects. The concentrations of PIIINP were significantly elevated in patients with ILD as compared to healthy subjects. In contrast, the concentration of APC-PCI and the values of APC-PCI/PC ratio were significantly decreased in BALF from patients with ILD. BALF concentration of PIIINP was significantly and inversely correlated with the concentration of APC-PCI and with the APC-PCI/PC ratio. These findings suggest that dysfunction of the protein C pathway may have important physiopathologic implications in the development of pulmonary fibrosis in ILD.

Biomarkers↗

PubMed2000

Listeriosis in a raccoon dog (Nyctereutes procyonoides) associated with canine distemper.

A wild raccoon dog (Nyctereutes procyonoides) that manifested severe illness and died was examined. Necropsy revealed severe emaciation, systemic icterus and petechial hemorrhages on the mucous membranes. Histopathologically, necroses were seen in the liver and brain stem associated with meningitis. Eosinophilic intranuclear inclusion bodies were observed in the spleen and intestinal mucosa, and eosinophilic intracytoplasmic inclusion bodies were seen in transitional epithelium in the bladder. Listeria monocytogenes 4b was isolated from the liver, spleen, kidneys and lungs, and the pathogen was also detected in the liver and brain stem immunohistopathologically. The disease was diagnosed as listeriosis associated with canine distemper virus infection in a raccoon dog.

Animals↗

PubMed2000

Recurrent spontaneous pneumothoraces associated with juvenile polymyositis.

A 17-year-old man, who had received a diagnosis of juvenile polymyositis (PM) at the age of 1 year, developed recurrent spontaneous pneumothoraces and underwent surgical treatment by means of video-assisted thoracic surgery. Intraoperative observation and microscopic studies demonstrated numerous bleb-like lesions below the visceral pleura. To our knowledge, this is the first article that describes a case of spontaneous pneumothorax associated with PM. Our observation should lead to broadening of the spectrum of pleuropulmonary manifestations of PM.

Adolescent↗