Objective To evaluate the role of CT and MR/in the diagnosis of posterior reversible encephalopathy syndrome(PRES).Methods Eight women with PRES(6 pregnant women,1 case after chemotherapy,and 1 patient with hypertension)were enrolled in our study.All of them had MR imaging (T_1WI,T_2WI,FLAIR,DWI),and five cases underwent post-contrast T_1WI and three dimensional contrast enhanced MR angiography(3D CEMRA).Two cases also had CT scan.Results MRV in all 8 patients showed no evidence of stenosis,dilation,or thrombosis in cranial veins and sinuses.MRI demonstrated multiple lesions located in bilateral parieto-occipital lobes(8 cases),bilateral basal ganglia(2 cases),and bilateral frontal lobes(4 cases).The lesions were prominent within white matter,some of them involved gray matter(3 cases).Lesions appeared as hyperintense signals on FLAIR and T_2-weighted images, isointense or mildly hypointense signals on T_1-weighted images,normal or decreased intensity on DWI,and isointensity or hyperintensity on apparent diffusion coefficient(ADC)maps.Post-contrast T_1WI showed mild reversible enhancement and 3D CEMFdisplayed numerous reversible“grape-like”enhancements in terminal arterial branches along the middle cerebral artery(MCA),anterior cerebral artery(ACA)and posterior cerebral artery(PCA).Follow-up scan showed decreased abnormal signals.Conclusion Lesions of PRES are usually located in parieto-occipital lobes,especially in white matter,but they can also be seen in frontal lobes and basal ganglia bilaterally.Post-contrast T_1WI and 3D enhanced MRA can provide useful information in the manifestation of reversible enhancement.MRI has advantages to display lesion in PRES,

This study was performed to investigate the subcellular changes of rat atrial muscle cells by immobilization stress. Sprague -Dawley rats weighting 200 gm were immobilized in small round plastic tube for 2, 6, 12, and 24 hours respectively. The atrial tissue obtained from each animals were observed by transmission electron microscopes. In the heart of rat subjected 2 hours immobilization stress no significant morphological changes were found in electron microscopy, similarly as in control animal. After 6 and 12 hours immobilization stress, the following electron -microscopic changes of atrial myocytes were observed at the swelling of mitochondrial matrix with disturbance in cristea, focal loss of cytoplasmic matrix, vacuoles with myeline -like structure, apoptotic changes of myocytes, focal widening of intercalated disc interspace and lysis of myofibrils. After 24 hours immobilization stress, very small sized mitochondria, similarly as small sized secretory granules and various sized granules are observed in the perinuclear region of atrial myocytes. Atrial specific granules are moved centripetally toward the central region of the atrial myocytes after immobilization stress. Above results will be aid in understanding the structures of atrium with dual function of blood circulation and endocrine, and in research of modulation of secretory granules in atrial muscle cells.
Animals ; Blood Circulation ; Cytoplasm ; Heart ; Immobilization* ; Microscopy, Electron ; Mitochondria ; Muscle Cells* ; Myelin Sheath ; Myofibrils ; Plastics ; Rats* ; Secretory Vesicles ; Vacuoles

BACKGROUND: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/J-Kit(W)/ Kit(W-v) (W/W(V)) and congenic normal WBB6F1/J-Kit +/+ (+/+) mice. METHODS: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, W/W(V) and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of W/W(V) and +/+ mice at 24 hours after 1% TDI challenge. RESULTS: TDI induced a significant ear swelling response in W/W(V) and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in W/W(V) and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus W/W(V) mice, either at baseline or after TDI-induced CHS. CONCLUSION: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.
Animals ; Asthma, Occupational ; Dermatitis, Contact* ; Dermis ; Ear ; Eosinophils ; Hypersensitivity ; Mast Cells ; Mice ; Models, Animal ; Neutrophils ; Skin ; Toluene 2,4-Diisocyanate ; Toluene*

BACKGROUND: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/J-Kit(W)/ Kit(W-v) (W/W(V)) and congenic normal WBB6F1/J-Kit +/+ (+/+) mice. METHODS: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, W/W(V) and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of W/W(V) and +/+ mice at 24 hours after 1% TDI challenge. RESULTS: TDI induced a significant ear swelling response in W/W(V) and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in W/W(V) and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus W/W(V) mice, either at baseline or after TDI-induced CHS. CONCLUSION: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.
Animals ; Asthma, Occupational ; Dermatitis, Contact* ; Dermis ; Ear ; Eosinophils ; Hypersensitivity ; Mast Cells ; Mice ; Models, Animal ; Neutrophils ; Skin ; Toluene 2,4-Diisocyanate ; Toluene*