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

Human seminal plasrna (HSP) is mixture of secretion derived from various glands associated with male reproductive tract which comprises approximately 80-90% of the volume of normal ejaculate. The present study was undertaken in an effort to explore the effect of HSP pretreatment on the production of IL-1B, TNF-a and IL-12, in mice, and to investigate if HSP may cause to induce active systemic anaphylaxis (ASA) in mice. In addition, effects of HSP pretreatment on contact hypersensitivity to trinitrochlorobenzene (TNCB), antibody response to polyvinylpyrroridone (PVP), a thymus-independent antigen and on ASA induced by egg albumin (OVA) were also studied in this study. For the experiments of contact hypersensitivity, antibody response and cytokine production, mice were pretreated i.p. daily with 0.3ml of HSP or sterile saline alone (control) for 3 consecutive days before antigen sensitization or lipopolysaccharide injection for the cytokine induction. For the experiments of OVA- induced anaphylaxis, mice were pretreated by a single s.c. injection of HSP 0.3ml per mouse before sensitization. For induction of ASA in mice by HSP, a group of mice were sensitized i.p. 2 consecutive days with 0.3ml of HSP and one day with 0.3 ml of HSP plus 2x10(9) B. pertussis and 1.0 mg of alum (schedule A) or another group of mice were sensitized i.p. with a single i.p. injection of 0.3 ml of HSP with 2x10' B. pertussis and 1.0 mg of alum (schedule B). All sensitized and unsensitized control mice were challenged i.v. with 0.2ml of HSP 14 days after HSP sensitization, and mortality were observed. It was found that HSP pretreatment inhibited the production of IL-lB, TNF-a and IL-12, and also inhibited OVA-induced ASA, contact hypersensitivity to TNCB and anti-PVP antibody production. Interestingly, ASA was induced by HSP irrespective of the applied sensitization schedule. Taken together, this study may provide the direct evidences that HSP may inhibit the production of IL-1B, TNF-a and IL-12 and this may be the first to show the induction of ASA by HSP in mice.
Anaphylaxis* ; Animals ; Antibody Formation ; Appointments and Schedules ; Dermatitis, Contact ; Humans* ; Interleukin-12 ; Male ; Mice* ; Mortality ; Ovum ; Picryl Chloride ; Semen* ; Whooping Cough

The pleomorphic adenoma is the most common neoplasm involving both the major and minor salivary glands. It is a benign, slowgrowing tumor, but local recurrences can occur. The pleomorphic adenoma gene 1 (PLAG1), which is a novel zinc finger gene, is frequently activated by reciprocal chromosomal translocations involving 8q12 in a subset of salivary gland pleomorphic adenomas. This experimental study was preformed to observe the translocation patterns between PLAG1 gene and the three translocation partner genes. We also have analyzed the presence of PLAG1 transcripts by RT-PCR. CTNNB1/PLAG1 gene fusion was observed in three of nine pleomorphic adnomas. However, LIFR/PLAG1 and SII/PLAG1 gene fusions were not detectable. All of three gene fusions was not detectable in one Warthin's tumor and three inflammatory salivary gland tissues. PLAG1 transcripts were expressed in all inflammatory salivary gland tissues and tumors except for three pleomorphic adenomas. Of particular one pleomorphic adenoma showing CTNNB1/P AG1 gene fusion did not express PLAG1 transcipt. Our data indicate that gene fusion involving PLAG1 is a frequent event in pleomorphic adenoma, but correlation between gene fusion involving PLAG1 and PLAG1 transcription is not definite.
Adenoma, Pleomorphic* ; Gene Fusion ; Recurrence ; Salivary Glands* ; Salivary Glands, Minor ; Translocation, Genetic ; Zinc Fingers

No abstract available.
Child* ; Humans ; Nephrotic Syndrome*

No abstract available.
Child* ; Humans ; Nephrotic Syndrome*

A prospective study was carried out to evaluate the validity of TROPT troponin T rapid assay in early diagnosis of acute myocardial infarction(AMI) in patients with ischemic chest pain, in comparison with conventional diagnostic tools such as serum troponin T(c-TnT) level, creatine Kinase(CK), CK-MB level and initial EKG finding. The study was performed at the emergency department(ED) of Yong Dong Severance hospital from March 1st 1996 to February 28th 1997. One hundred eighty one patients visiting ED with chief complaint of atraumatic chest pain within 24 hours of visit were eligible for the study. Those who lacked enough data collection and those who had chest paint of noncardiac origin and EKG of PSVT were excluded from the study. The overall study population was a total of 131 patients. Initial EKG, TROPT rapid assay, CK, CK-MB and c-TnT level were obtained simultaneously. Diagnosis of AMI was made according to the international diagnostic criteria for AMI. Of the 131 patients 61 patients(46.6%) were diagnosed as AMI. Within 4 hours of their symptom onset, initial EKG showed the highest sensitivity(63.2%) whereas the sensitivities of TROPT rapid assay, c-TnT, CK and CK-MB were poor(0-0.7%). From 4-8 hours, the sensitivities of c-TnT, CK and CK-MB were higher than that of TROPT rapid assay(80% vs. 30%). The sensitivites of TROPT rapid assay, c-TnT, CK and CK-MB rose over time and reached 100% after 8 hours symptom onset. The specificities of the TROPT rapid assay, c-TnT, CK & CK-MB and EKG were all 100% within 8 hours after symptom onset. Discrepancy between TROPT rapid assay and c-TnT was noted in nine patients(6.9%). In this study TROPT rapid assay was valuable in the diagnosis of AMI after 8 hours of symptom onset.
Chest Pain* ; Creatine ; Data Collection ; Diagnosis ; Early Diagnosis ; Electrocardiography ; Emergencies ; Humans ; Paint ; Prospective Studies ; Thorax* ; Troponin ; Troponin T

No abstract available.
Cholangitis*

No abstract available.
Dislocations* ; Tendons*

No abstract available.
Tibial Fractures*

No abstract available.
Animals ; Cerebellum* ; Inositol 1,4,5-Trisphosphate* ; Inositol* ; Rats*