No abstract available.
Arthrography* ; Wrist*

No abstract available.
DNA* ; Lung Neoplasms* ; Lung* ; Ploidies*

No abstract available.
Heart Diseases* ; Heart*

No abstract available.
Animals ; Cryopreservation* ; Embryonic Structures* ; Mice* ; Ovum*

Focal segmental glomerulosclerosis (FSGS) is characterized by focal and segmental obliteration of glomerular capillary tufts with increased matrix. FSGS is classified as collapsing, tip, cellular, perihilar and not otherwise specified variants according to the location and character of the sclerotic lesion. Primary or idiopathic FSGS is considered to be related to podocyte injury, and the pathogenesis of podocyte injury has been actively investigated. Several circulating factors affecting podocyte permeability barrier have been proposed, but not proven to cause FSGS. FSGS may also be caused by genetic alterations. These genes are mainly those regulating slit diaphragm structure, actin cytoskeleton of podocytes, and foot process structure. The mode of inheritance and age of onset are different according to the gene involved. Recently, the role of parietal epithelial cells (PECs) has been highlighted. Podocytes and PECs have common mesenchymal progenitors, therefore, PECs could be a source of podocyte repopulation after podocyte injury. Activated PECs migrate along adhesion to the glomerular tuft and may also contribute to the progression of sclerosis. Markers of activated PECs, including CD44, could be used to distinguish FSGS from minimal change disease. The pathogenesis of FSGS is very complex; however, understanding basic mechanisms of podocyte injury is important not only for basic research, but also for daily diagnostic pathology practice.
Actin Cytoskeleton ; Age of Onset ; Capillaries ; Diaphragm ; Epithelial Cells ; Foot ; Glomerulosclerosis, Focal Segmental* ; Nephrosis, Lipoid ; Pathology ; Permeability ; Podocytes ; Rabeprazole ; Sclerosis ; Wills

To attempt a rigorous definition of the structure of the accessory spleen (AS) in the Chinese hamster, we examined twenty-one animals, and found AS in 5 animals (23.8%), which were over 7-month-old. The AS had no connection with the main spleen and was seen as a dark red oval organ (0.7 mm x 1.5 mm), which was embedded in the adipose tissue near the tail of the pancreas. It was demarcated from the adipose tissue and some pancreatic tissue. The organ was encapsulated by thin collagenous connective tissue and smooth muscle fibers, and contained lymphatic nodules, reticular fibers, nodular central arterioles, macrophages and megakaryocytes. Notably the incidence of AS appeared to increase with age in the Chinese hamsters.
Adipose Tissue/anatomy & histology ; Age Factors ; Animals ; Connective Tissue/anatomy & histology ; Cricetinae ; Cricetulus/*anatomy & histology ; Erythrocytes/cytology ; Lymphocytes/cytology ; Muscle, Smooth/anatomy & histology ; Pancreas ; Spleen/*anatomy & histology/cytology

No abstract available.
Hydroxyurea ; Hyperpigmentation*

No abstract available.
Onycholysis*

To find out the predictors of nocturnal arterial oxygen desaturation in patients with respiratory diseases, transcutaneous oxygen saturation(StcO2) monitoring studies using a pulse oximeter were performed during sleep in 20 patients. StcO2 was decreased more than 4% from the baseline value in 18 patients(90%) and more than 10%('Desaturator') in 8(40%). Five of the seven patients(71.4%) with awake PaO2<60mmHg and three of the thirteen patients(23.1%) with awake PaO2≥60mmHg were 'desaturators'. The awake PaO2/FIO2 and PaO2/PAO2 could distinguish 'desaturator' from 'nondesaturator, and PaO2, SaO2 or StcO2 could not. These results suggest that the nocturnal oxygen desaturation depends on the severity of the underlying disease rather than the baseline PaO2. Anthropomorphic and lung function factors could not separate between 'desaturator' and 'non-desaturator', and about a quarter of patients with a wake PaO2≥60mmHg developed significant desaturation. Therefore, it is necessary to monitor the nocturnal arterial oxygen saturation in patients with respiratory diseases regardless of their severity of airflow obstruction or awake PaO2.
Humans ; Lung ; Oxygen*

We experienced a case of primary malignant mixed mullerian tumors (MMMT) of the fallopian tube of FIGO stage I. In addition to endometrioid adenocarcinomas, multiple apparent heterologous elements encompassing myxoid chondrosarcoma, osteosarcoma, myxoid liposarcoma and well differentiated angiosarcoma were recognized as separate nodules. These findings have not been described previously in MMMTs of the female genital tract.
Carcinoma, Endometrioid ; Chondrosarcoma ; Fallopian Tubes* ; Female ; Hemangiosarcoma ; Humans ; Liposarcoma, Myxoid ; Osteosarcoma