No abstract available.
Animals ; Capsaicin* ; Colon* ; Cytokines* ; Lung* ; Melanoma, Experimental* ; Mice* ; RNA, Messenger*

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

Septic shock is one of the leading cause of death in hospitalized patients and mortality rates of up to 50 % have been reported. Despite all efforts, no regimen today seems to be successful in the treatment of septic shock. The endogenous opioid system (EOS) includes three major families of peptides: dynorphins, endorphins and enkephalins. Several lines of evidence indicate that EOS is implicated in the pathophysiology of anaphylactic and endotoxic shock. An opioid receptor blocker naloxone has been used extensively in studies for the role of EOS or endogenous opiod peptides (EOP). However, there have been few, if any, detailed investigative studies regarding the effect of naloxone on TNF-a production and the lethality in response to endotoxin, and tumorigenesis. ...continue...
Carcinogenesis* ; Cause of Death ; Dynorphins ; Endorphins ; Enkephalins ; Humans ; Melanoma ; Mortality ; Naloxone* ; Nitric Oxide ; Peptides ; Receptors, Opioid* ; Shock, Septic*

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

No abstract available.
Herpesvirus 4, Human*

No abstract available.
Adaptive Immunity ; Animals ; Cell Line* ; Rats*

No abstract available.
Antibodies, Monoclonal* ; Herpesvirus 4, Human* ; Humans* ; Tetanus Toxoid* ; Tetanus*

Actinomycosis, in which the principal causative agent in man is known to Actinomyces israelii, is a chronic, suppurative diseases characterized by extensive fibrosis, multiple abscesses, and formation of sinus tracts that drain suppurative exudates. On the basis of the anatomical sites involved; it can be subclassified into the cervicofacial form, which is the most common form, pulmonary form and abdominal form. Kidneys are rarely affected. Clinically, radiologically, and at operation it is difficult to differentiate the renal actinomycosis from renal tuberculosis and renal carcinoma. The prognosis is excellent after nephrectomy followed by appropriate antibiotic therapy. We presented a case of renal actinomycosis with a brief review of the literatures.
Male ; Humans

No abstract available.
Wounds and Injuries

No abstract available.
Eosinophilic Granuloma* ; Eosinophils* ; Meningitis, Bacterial*