Neurocognitive and psychiatric disorders-related axonal degeneration in Parkinson's disease

Neurocognitive and psychiatric disorders have significant consequences for quality of life in patients with Parkinson's disease (PD). In the current study, we evaluated microstructural white matter (WM) alterations associated with neurocognitive and psychiatric disorders in PD using neurite orientation dispersion and density imaging (NODDI) and linked independent component analysis (LICA). The indices of NODDI were compared between 20 and 19 patients with PD with and without neurocognitive and psychiatric disorders, respectively, and 25 healthy controls using tract-based spatial statistics and tract-of-interest analyses. LICA was applied to model inter-subject variability across measures. A widespread reduction in axonal density (indexed by intracellular volume fraction [ICVF]) was demonstrated in PD patients with and without neurocognitive and psychiatric disorders, as compared with healthy controls. Compared with patients without neurocognitive and psychiatric disorders, patients with neurocognitive and psychiatric disorders exhibited more extensive (posterior predominant) decreases in axonal density. Using LICA, ICVF demonstrated the highest contribution (59% weight) to the main effects of diagnosis that reflected widespread decreases in axonal density. These findings suggest that axonal loss is a major factor underlying WM pathology related to neurocognitive and psychiatric disorders in PD, whereas patients with neurocognitive and psychiatric disorders had broader axonal pathology, as compared with those without. LICA suggested that the ICVF can be used as a useful biomarker of microstructural changes in the WM related to neurocognitive and psychiatric disorders in PD.     

Selective embolization of the splenic vein in patients with hepatic encephalopathy and splenorenal shunt

Obliteration of portal-systemic shunts is effective for portosystemic encephalopathy but is often associated with complications such as retention of ascites and worsening of esophageal varices. Selective embolization of the splenic vein was performed on six patients with hepatic encephalopathy and splenorenal shunts. Hepatic encephalopathy was not observed in four patients after the procedure. Neither retention of ascites nor rupture of esophageal varices was observed because postoperative elevation of portal venous pressure was not as great as that seen when shunt obliteration is performed. This procedure can be an effective and safe treatment option for hepatic encephalopathy with a splenorenal shunt.     

Spontaneous pneumothorax in pregnancy: a case report and review of the literature

Spontaneous pneumothorax in pregnancy is said to be a rare condition. A 37-year-old woman at 13 weeks' gestation with this rare complication, was reported. The patient was first treated by chest tube drainage, which failed to get complete reexpansion of the lung, and she was managed by thoracotomy twenty days after. She delivered, at full term, a healthy normal infant by cesarean section. Indications for operative treatment of pneumothorax in pregnancy, in general, are not absolutely defined. We believe that the usually accepted indications for operation, such as persistence of air leakage despite adequate drainage and multiple recurrences of pneumothorax, are valid during pregnancy, if the patient allows the pregnancy to proceed.     

The Role of Diagnostic Radiology Including Lymphography in Malignant Lymphomas

Among the applications of diagnostic radiology in malignant lymphoma, G.I. examination and lymphography have been discussed. It is extremely important to accurately evaluate the extent of the lesion by use of radioisotopes as well as other X-ray studies. Since the disease is characterised by a high radiosensitivity, adequate radiation therapy should result in some healing and a prolongation of life even in advanced cases. Diagnosis and treatment are quite intimately related in this disease.     

Risk factors for deterioration of long-term liver function after radiofrequency ablation therapy

AIM:To identify factors that influence long-term liver function following radiofrequency ablation(RFA)in patients with viral hepatitis-related hepatocellular carcinoma.METHODS:A total of 123 patients with hepatitis B virus-or hepatitis C virus-related hepatocellular carcinoma(HCC)(n=12 and n=111,respectively)were enrolled.Cumulative rates of worsening Child-Pugh(CP)scores(defined as a 2-point increase)were examined.RESULTS:CP score worsening was confirmed in 22patients over a mean follow-up period of 43.8±26.3mo.Multivariate analysis identified CP class,platelet count,and aspartate aminotransferase levels as significant predictors of a worsening CP score(P=0.000,P=0.011 and P=0.024,respectively).In contrast,repeated RFA was not identified as a risk factor for liver function deterioration.CONCLUSION:Long-term liver function following RFA was dependent on liver functional reserve,the degreeof fibrosis present,and the activity of the hepatitis condition for this cohort.Therefore,in order to maintain liver function for an extended period following RFA,suppression of viral hepatitis activity is important even after the treatment of HCC.     

A case of spontaneous resolution of sarcoidosis with primary pulmonary cavitations]

On routine physical checkup, a 27-year-old man with productive cough was found to have multiple nodules with cavitation in the bilateral lung fields and mediastinal and hilar lymph adenopathy on chest X-ray film and CT scan. Serum levels of angiotensin converting enzyme and lysozyme were high. Tuberculin reaction was negative. Non-caseous epitheloid granulomas were confirmed in the bronchial wall specimens obtained by trans-bronchial biopsy. The number of lymphocytes and the CD4/CD8 ratio of lymphocytes in bronchoalveolar lavage fluid was increased. Therefore, pulmonary sarcoidosis was diagnosed, and the lung nodules with cavitation were considered due to sarcoidosis. The walls of the cavitations gradually thinned and had almost completely vanished after 6 months of careful observation without steroid therapy.     

Identification of metabolites of NK-104, an HMG-CoA reductase inhibitor, in rat, rabbit and dog bile

NK-104 is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase with a very potent lipid-lowering effect. Biotransformation profiles of NK-104 in bile from rat, rabbit and dog given an intravenous infusion of NK-104 were investigated. Structural assignment was made by liquid chromatography (LC)-mass spectrometry (MS)-MS and proton NMR analyses. The predominant component was intact NK-104 in all the animals. At least eight other metabolites were present in rat, four in rabbit, and 10 in dog. These bile metabolites were purified and isolated by preparative HPLC. Biotransformation pathways elucidated for NK-104 were as follows: (a) lactonization ; (b) beta-oxidation of the side-chain; (c) hydroxylation of the quinoline ring; (d) conjugation with Beta-glucuronic acid and taurine. Beta-oxidative degradation of the side-chain in the case of other HMG-CoA reductase inhibitors is necessary for epimerization of the hydroxy group which has an R-configuration. However, M-16, glucuronide of the ketolactone derivative, was obtained as a key metabolite suggesting another beta-oxidation pathway for the side-chain.     

A case of pneumocystis carinii pneumonia associated with low dose methotrexate treatment for rheumatoid arthritis and trimethoprim-sulphamethoxazole induced pancytopenia]

A 64-year-old man was admitted to our hospital complaining of dyspnea and fever. He had been treated with low-dose methotrexate for rheumatoid arthritis. Chest radiography showed diffuse ground-glass attenuation in both lung fields, and hypoxia was detected. Pneumosystis carinii pneumonia was demonstrated on transbronchial lung biopsy, and the serum beta-D glucan level was high. We started treatment with trimethoprim-sulphamethoxazole, but respiratory failure worsened, and drug-induced pancytopenia occurred. Although trimethoprim-sulphamethoxazole was stopped, pancytopenia persisted and the patient required ventilatory support. After we changed the medication from trimethoprim-sulphamethoxazole to pentamidine, respiratory failure improved. It was thought that pneumocystis carinii pneumonia was associated with low-dose methotrexate and that trimethoprim-sulphamethoxazole interacted with methotrexate to induce severe pancytopenia.