No abstract available.

No abstract available.
Diagnosis* ; Ossification, Heterotopic* ; Risk Factors* ; Spinal Cord Injuries* ; Spinal Cord*

No abstract available.
Orbit*

A case of pulmonary alveolar proteinosis is reported. Most of the alveolar spaces were filled with amorphous deep eosinohilic material which revealed strong positive reaction to periodic acid-Schiff staining. Electron microscopic observation of this material showed numerous lamellar bodies in the alveolar spaces and cytoplasms of alveolar macrophages. A part of them were concentric multilamellated type A lamellar bodies and the other were finger printlike type B bodies. Combined type A and type B lamellar bodies were rarely present. From the above features it is suggested that both type A and B lamellar bodies could be transformed one another and those lamellar bodies may be originated from pulmonary surfactant.

Subcutaneous fat necrosis of the newborn is an uncommon disorder characterized by firm b-cutaneous plaques and nodules usually appearing shortly after birth. It runs a relatively be, n course and may completely resolve in a few months without any recurrence. We report a case of subcutaneous fat necrosis in a 15 day-old male suffering from severe p inatal asphyxia and hypoxic cardiomyopathy, who presented with indurated subcutane s nodules and plaques on the both shoulders and the back. Histologically the subcutaneous fat showed focal necrosis with needle-shaped clefts, lymphohistiocytic infiltration and foreign body reactions consistent with subcutaneous fat necrosis of the newborn. In our patient, compromised cardiac output due to cardiomyopathy might have aggravated hypoxic condition and it could be speculated that cardiomyopathy-induced systemic hypoxia gave rise to hypothermia of the skin as a result of peripheral vasoconstriction. This report presents a causal relationship of cardiomyopathy and subcutaneous fat necrosis of the newborn.
Anoxia ; Asphyxia ; Cardiac Output ; Cardiomyopathies* ; Foreign Bodies ; Humans ; Hypothermia ; Infant, Newborn* ; Male ; Necrosis* ; Parturition ; Recurrence ; Shoulder ; Skin ; Subcutaneous Fat* ; Vasoconstriction

No abstract available.
Fibronectins* ; Granulation Tissue* ; Wound Healing* ; Wounds and Injuries*

Perianal fistula is a frequent complication and one of the subclassifications of Crohn disease (CD). It is the most commonly observed symptomatic condition by colorectal surgeons. Accurately classifying a perianal fistula is the initial step in its management in CD patients. Surgical management is selected based on the type of perianal fistula and the presence of rectal inflammation; it includes fistulotomy, fistulectomy, seton procedure, fistula plug insertion, video-assisted ablation of the fistulous tract, stem cell therapy, and proctectomy with stoma creation. Perianal fistulas are also managed medically, such as antibiotics, immunomodulators, and biologics including anti-tumor necrosis factor-alpha agents. The current standard treatment of choice for perianal fistula in CD patients is the multidisciplinary approach combining surgical and medical management; however, the rate of long-term remission is low and is reported to be 50% at most. Therefore, the optimum management strategy for perianal fistulas associated with CD remains controversial. Currently, the goal of management for CD-related perianal fistulas are controlling symptoms and maintaining long-term anal function without proctectomy, while monitoring progression to anorectal carcinoma. This review evaluates perianal fistula in CD patients and determines the optimal surgical management strategy based on recent evidence.

BACKGROUND: Heparin-induced thrombocytopenia/ thrombosis (HITT) is recognized as the most frequent and fatal symptom complexes in patients receiving heparin therapy. The antibodies of HITT are not directly bound to heparin but bound to complexes of heparin and platelet factor 4 (PF4) derived from platelet alpha-granules. That is, HITT IgG antibody-heparin-PF4 immune complexes are bound to FcgammaRII receptor of platelets, which induced thrombocytopenia. Some researches showed the antibodies reactive to platelets could be IgM or IgA as well as IgG. So in this study, the authors tried to explain the molecular basis of heparin-PF4-isoantibody complexes . METHODS: In HITT patients who had received long-term heparin therapy, we determined HITT isoantibodies and titers using heparin:PF4 ELISA. When fifteen HITT patients with high titer antibodies (more than 1 : 100) were selected, reaction patterns of isoantibodies with the platelets were examined through serotonin release test and flow cytometry. RESULTS: All patients showed one or more isotype antibodies and the most frequent isotype was IgGl (nine patients) . In the presence of optimal concentra pion of heparin and PF4, ten patients had antibodies which activated platelets, and all of them were positive in serotonin release test. Reactive plasmas had IgGl, IgG3, IgA or IgM antibodies, and each of them except one had IgGl. These platelet activations could be blocked in vitro by anti-IV.3 antibody. Non-reactive plasmas were negative In serotonin release assay nor had TgGl. The plasmas 4hat had two or more isoantibodies showed a similar pattern of the IgG antibody by flow cytometry. CONCLUSIONS: The HITT antibodies can be all kinds of antibody isotopes, but IgA and IgM may not bind to the platelets directly. It seems to be possible only after reacting with heparin-PF4-IgG complexes.
Antibodies ; Antigen-Antibody Complex ; Blood Platelets ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Heparin ; Humans ; Immunoglobulin A ; Immunoglobulin G ; Immunoglobulin M ; Isoantibodies ; Isotopes ; Mesons ; Plasma ; Platelet Activation ; Platelet Factor 4 ; Serotonin ; Thrombocytopenia ; Thrombosis*

Acute disseminated encephalomyelitis(ADEM) and acute relapsing disseminated encephalomyelitis(ARDEM) are representative demyelination diseases that occur among young children with a fulminant onset similar to encephalitis or meningitis. The diseases often occur after some viral infection of immunization and the etiology of these diseases is considered to be an autoimmune response because of the similarity in pathologic findings to experimental allergic encephalomyelitis. Cerebral computed tomography(CT) findings of demyelination in ADEM or ARDEM show normal to low density areas in the white matter. In cerebral MRI findings, a scattered distinct high intensity lesion considered to be demyelination is observed in 72-weighted imaging even in the early stages. ADEM is usually monophasic, but recurrent episodes may occure. When ADEM is reccurent, the distinction from multiple sclerosis becomes difficult. We report here a case of acute relapsing disseminated encephalomyelitis(ARDEM) in a 9 years old male child who experence ADEM, 3 times.
Autoimmunity ; Child ; Demyelinating Diseases ; Encephalitis ; Encephalomyelitis, Acute Disseminated* ; Encephalomyelitis, Autoimmune, Experimental ; Humans ; Immunization ; Magnetic Resonance Imaging ; Male ; Meningitis ; Multiple Sclerosis

No abstract available.