No abstract available.
Evoked Potentials, Somatosensory* ; Transcutaneous Electric Nerve Stimulation*

No abstract available.
Hemorrhoids*

No abstract available.
Rectal Neoplasms*

No abstract available.
Hemorrhoids*

No abstract available.
Rectal Neoplasms*

No abstract available.
Overbite*

No abstract available.
Peroneal Nerve*

No abstract available.
Rehabilitation* ; Stroke*

Alveolar macrophages participate in the host defense against P. carinii, but the mechanisms in degradation and clearance of the organism from lung has not been well established. We observed the transmission and scanning electron microscopic features and evaluated the expression of TNF-alpha and Surfactant-D in the interaction of P. carinii with alveolar macrophages. Expression of TNF-alpha and Surfactant-D in the experimentally induced P. carinii pneumonia in rat was examined by immunohistochemistry and immunoelectron microscopy. Electron microscopically, the alveolar macrophages phagocytized trophozoites and cysts of P. carinii micro-organisms. Immunohistochemically TNF-alpha was strongly expressed in the cytoplasms of alveolar macrophages. Postembedding immunogold labeling for Surfactant-D protein was expressed on the pellicles of trophozoites and cysts, P. carinii micro-organisms in the cytoplasms of macrophages, free floating surfactant materials and multilamellar bodies of type II epithelial cells. We conclude that alveolar macrophages interacted with P. carinii micro-organisms respond with increased expression of TNF-alpha. TNF-alpha may bind to P. carinii and exert a direct toxic effect upon the micro-organisms. Surfactant-D protein may augment binding of P. carinii to the alveolar macrophages and enhance the clearance of the micro-organisms.
Animals ; Cytoplasm ; Epithelial Cells ; Immunohistochemistry ; Lung ; Macrophages ; Macrophages, Alveolar* ; Microscopy, Immunoelectron ; Pneumocystis carinii* ; Pneumocystis* ; Pneumonia ; Pneumonia, Pneumocystis* ; Rats ; Trophozoites ; Tumor Necrosis Factor-alpha*

Lupus vulgaris is most prevalent on exposed parts, especially the face but can also develop on exetremities. Lupus vulgaris originates from tuberculosis elsewhere in the body by hematogenous, lymphatic, or contiguous spread. A 19-year-old male patient came to our department. The patient had had many recurrent oozing and verrucous plaques and crusts on the left foot for one year. A skin biopsy from the lesion on the left dorsum of the foot showed scattered well defined granulomas consisting of the epithelioid cell clusters with Langerhans and foreign body type giant cells in the mid dermis. Caseation necrosis was slight. There were no bacilli on AFB staining. The multi test CMI for tuberculin was highly positive. A chest X-ray did not show any abnormal findings. The presence of Mycobacterium tuberculosis DNA was demonstrated by polymerase chain reactions (PCR) for detection of mycobacterial DNA from a routinely prepared paraffin-embedded skin specimen. Herein we report a very atypical case of lupus vulgaris confirmed by PCR.
Biopsy ; Dermis ; DNA ; Epithelioid Cells ; Foot ; Giant Cells, Foreign-Body ; Granuloma ; Humans ; Lupus Vulgaris* ; Male ; Mycobacterium tuberculosis ; Necrosis ; Polymerase Chain Reaction ; Skin* ; Thorax ; Transplants* ; Tuberculin ; Tuberculosis ; Young Adult