A case of congenital self-healing histiocytosis was studied with S-100 antibody and electron microscopy. Many tumor cells were positive for S-100 protein and a few contained Birbeck´s grandles and dense bodies. A pathlogic fracture was first noticed on the seventh day. The lesions involuted spontaneously by the end of a weeks
Histiocytosis* ; Microscopy, Electron ; S100 Proteins

No abstract available.
Colon*

No abstract available.
Child* ; Humans

Seven patients with aortic valve vegetation were examined by M-mode and two dimensional echocardiography. Underlying cardiac abnormalities were found in 6 patients, four had rheumatic heart disease, one had congenital bicuspid aortic valve, one had coexistence of asymmetrical septal hypertrophy and aortic regurgitation. Aortic regurgitation were found in all patients. One of seven patients had cerebral embolization and all patients had overt congestive heart failure. Of 5 patients medically treated, three became moribund, one died and one improved clinically. One patient underwent cardiac surgery, the aortic cusps were congenital bicuspid with vegetation, aortic valve replacement was successful. Echocardiogram of 7 patients with aortic valve vegetation showed characteristic shaggy, irregular mass of echoes produced by vegetation in the aortic valve during systole and diastole. Two of seven patients had abnormal mass of echoes in the left ventricular outflow tract. During systole, two had vegetation on the right coronary cusp and one had vegetation on the noncoronary cusp by M-mode echocardiography. In other patients we could not localize invoving aortic cusps by M-mode echocardiogram. All patients had left ventricular volume overload. For of seven patients had fluttering of anterior mitral valve. Two had fluttering of interventricular seputm. Five had premature mitral valve closure before QRS complex.
Aortic Valve Insufficiency ; Aortic Valve* ; Bicuspid ; Diastole ; Echocardiography* ; Heart Failure ; Humans ; Hypertrophy ; Mitral Valve ; Rheumatic Heart Disease ; Systole ; Thoracic Surgery

No abstract available.
Humans ; Infant*

No abstract available.
Weaning*

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Animals ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Humans ; Lymph Nodes ; Mice ; Prostaglandins E ; Skin ; Tissue Donors

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Animals ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Humans ; Lymph Nodes ; Mice ; Prostaglandins E ; Skin ; Tissue Donors

No abstract available.
Edema* ; Hydrops Fetalis*

Allergic disease is a complex disorder in which the interaction between environmental and genetic effects may modify both the susceptibility to and severity of the disease. Over the last few years, our understanding of the genetic basis of allergic diseases has improved markedly, which has led to the identification of several chromosome regions and loci showing linkage to allergic disease. As another approach, association studies between candidate gene polymorphisms and allergic diseases have been conducted in many areas and replicated in different ethnic groups. These approaches need to be followed by validation processes to confirm their functional relevance in the pathophysiology of allergic disease. This review updates genetic studies of and recent findings in, allergic disease.
Ethnic Groups ; Humans