No abstract available.

It has been known that the interconnection between the gervous, endocrine and immune system are largely mediated through regulatory soluble factors such as neruopeptides, cytokines and hormones. Capsaicin, the pungent principle of hot peppers, is a neurotoxin that affects primary sensory neurons of the C and A-b type and depletes primary sensory neurons (polymodal nociceptors) of neuropeptides like tachykinin. In this study capsaicin was used to explore the possible role of the neruons on the expression of cellular and humoral immune responses and TNF-a prodcution. Mice were pretreated with s.c. injections in the neck region with a single dose of 100 u,g of capsaicin per mouse before immunization. ...continue...
Anaphylaxis* ; Animals ; Capsaicin* ; Carcinogenesis* ; Cytokines ; Immune System ; Immunity, Humoral ; Immunization ; Mice* ; Neck ; Neuropeptides ; Sensory Receptor Cells ; Tachykinins

No abstract available.
Diabetic Neuropathies ; Humans

Acoustics ; Child ; Cleft Palate ; Humans ; Korea

Inflammatory myofibroblastic tumor (IMT) is a space occupying lesion which is composed of myofibroblasts, plasma cells, and lymphocytes. IMT of the maxillary sinus is rare and its etiology is unknown. We present a case of inflammatory myofibroblastic tumor occurring in the right maxillary sinus of a 57-year-old woman. Radiologically, this tumor was interpreted as malignant neoplasm. On histologic examination, bundles of spindle cells were admixed with inflammatory cells including mature plasma cells and lymphocytes. On the basis of the immunohistochemical findings and ultrastructural features, we recognized that the intervening spindle cells were myofibroblasts. We discussed etiology and prognostic factors of this tumor.
Female ; Humans ; Lymphocytes ; Maxillary Sinus* ; Middle Aged ; Myofibroblasts* ; Plasma Cells

Carotidynia is defined as an atypical craniofacial pain syndrome caused by the dilatation or distension of the extracranial arteries. We report an unusual case of carotidynia mimicking trigeminal neuralgia caused by an arterioscle-rotic tortous carotid artery. A 68-year-old woman suffered from frequent episodes of severe electrical shock-like radiating pain around her left ophthalmic and maxillary division of the trigeminal nerve for 5 years. Initially, under the impression of trigeminal neuralgia, carbamazepine was tried. She was reevaluated due to an unsatisfactory pharmacological response. On examination, no abnormalities were found on the craniofacial region except for a tortous pulsating tender mass on the region of the left carotid artery. Routine laboratory findings and a connective tissue study were normal. Neck sonography and a 4-vessel angiography showed a tortous left internal carotid artery with stenosis extending near to the skin. The patient was treated for 2 weeks with a nonsteroidal anti-inflammatory agent, steroids, a prophylctic beta blocker, and a TCA antidepressant. The pain gradually subsided.
Aged ; Angiography ; Arteries ; Carbamazepine ; Carotid Arteries ; Carotid Artery, Internal ; Connective Tissue ; Constriction, Pathologic ; Dilatation ; Facial Neuralgia ; Female ; Humans ; Neck ; Skin ; Steroids ; Trigeminal Nerve ; Trigeminal Neuralgia*

No abstract available.
Adult ; Humans ; Male

Macrophage colony-stimulating factor (M-CSF) is known as one of the factors essential for osteoclast development. In the present study, we examined effects of M-CSF on the apoptotic pathway of osteoclast precursors and their underlying molecular mechanisms. Osteoclast precursors underwent apoptosis in the absence of M-CSF, even in the presence of receptor activator of NF-kB ligand (RANKL). Active caspase-3 and -9 were detected in the osteoclast precursors and treatments of precursors with their specific inhibitors (Z- DEVD-FMK and Z-LEHD-FMK) decreased the apoptosis. M-CSF decreased apoptosis in a dose-dependent manner with decreasing in active caspases-3 and -9 levels and up-regulating Bcl-XL. Those effects of M-CSF on inhibiting apoptosis of osteoclasts precursor by regulating anti-apoptotic signals was more effective when combined with RANKL. These results demonstrate that M-CSF acts as a survival factor for the osteoclast precursors. Furthermore, it is believed that the apoptosis of osteoclast precursors may be involved in the activation of caspase-9 and that M-CSF may promote their survival through Bcl-XL-induced inhibition of caspase-9 activation.
Animals ; Apoptosis/drug effects/physiology ; Carrier Proteins/pharmacology ; Caspases/antagonists & inhibitors/drug effects/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Activation/drug effects ; Female ; Macrophage Colony-Stimulating Factor/*pharmacology ; Membrane Glycoproteins/pharmacology ; Mice ; Mice, Inbred ICR ; Oligopeptides/pharmacology ; Osteoclasts/*cytology/drug effects ; Proto-Oncogene Proteins c-bcl-2/drug effects/*metabolism ; Stem Cells/cytology/*drug effects ; Up-Regulation

No abstract available.
Giant Cell Arteritis*

The anesthetic properties on blockade of tourniquet pain of hyperbaric tetracaine (T-caine) and bupivacaine (marcaine) with or without epinephrine administered intrathecally were compaired in randomized study involving fourty healthy surgical patients. This investigation employed solutions of the two agents with or without epinephrine that contained equal dose (13 mg), concentration (0.5%), and volume (3ml). No statistically significant difference in height, anesthetic time, tourniquet time, tourniquet pressure, and sensory blockade level were observed between the four groups. Tourniquet pain or inadequate anesthesia did not occur in epinephrine-mix groups, But occurred in 20% of the patients in the tetracaine (t-caine) group & bupivacaine (marcaine) group each other. The results suggest that equal concentrations and dosages of hyperbaric tetracaine (T-caine) and bupivacaine (Marcaine) possessed similar anesthetic qualities on blockade of tourniquet pain following subarachnoid administration.
Anesthesia ; Bupivacaine* ; Epinephrine ; Humans ; Tetracaine* ; Tourniquets*