ABSTRACT
The nerves innervating the auricle of the rat were investigated using PRV (pseudorabies virus) as a neural tracer. The neural tracer was injected into rostral part of the right auricle of the rat. The PRV immunoreactive neurons were labeled bilaterally and more densely labeled in the brain than spinal cord. In the brain, PRV immunoreactive neuronal cell bodies and fibers were observed in thalamus, periaqueductal gray matter, reticular formation, spinal trigeminal nucleus, spinal tract of trigeminal nerve and facial nucleus. The more densely labeled PRV immunoreactive neurons were found in thalamus, reticular formation, spinal tract of trigeminal nerve and facial nucleus. In the spinal cord, PRV immunoreactive neurons were extended from T8 to L2 segments. The more densely labeled PRV immunoreactive neurons were found from T11 to L2 segments. Above results, the nerves innervating the auricle of the rat were widely distributed in brain and spinal cord and may have many connections with other nerves. These results may provide a neuroanatomical data on the nerves innervating the auricle of the rat in the central nervous system.
Subject(s)
Animals , Rats , Brain , Central Nervous System , Herpesvirus 1, Suid , Neurons , Periaqueductal Gray , Reticular Formation , Spinal Cord , Thalamus , Trigeminal Nerve , Trigeminal Nucleus, SpinalABSTRACT
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.
Subject(s)
Animals , Mice , Asthma, Occupational , Dermatitis, Contact , Dermis , Ear , Eosinophils , Hypersensitivity , Mast Cells , Models, Animal , Neutrophils , Skin , Toluene 2,4-Diisocyanate , TolueneABSTRACT
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.
Subject(s)
Animals , Mice , Asthma, Occupational , Dermatitis, Contact , Dermis , Ear , Eosinophils , Hypersensitivity , Mast Cells , Models, Animal , Neutrophils , Skin , Toluene 2,4-Diisocyanate , TolueneABSTRACT
PURPOSE: We report clinical and radiological results of 32 HA-coated femoral implants at midterm follow-up. MATERIALS AND METHODS: We reviewed 25 patients (32 hips) treated with HA-coated femoral implants from April 1992 to october 1993. The follow up period was five to six years (average 64.5 months) RESULTS: Harris hip score averaged 93 at the most recent follow-up examination. At the last follow-up, three patient suffered mild thigh pain, but experienced no trouble in daily activity. In radiological evaluation, the endosteal bone formation was noted mostly in Gruen zone 2 and 6 of HA-coated area. The radiolucent line was noted mostly in Gruen zone 4 of uncoated area. Enghs radiological score was increased in fixation scale but decreased in stability scale during the follow-up period. CONCLUSIONS: HA-coated component provides early pain relief and satisfactory radiological result. However, a longer follow-up is required to determine whether the favorable results of HA-coated implant are maintained or not.